Anthocyanins and liver detoxification -
Many studies have demonstrated that anthocyanins reduce inflammation systemically, including in adipose fat tissue. This fact is particularly insightful for cases of Non-alcoholic fatty liver disease NAFLD , where inflammation can be damaging to the liver.
Inflamed tissue often contains a type of white blood cell that perpetuates the inflammation. NAFLD is on the rise due to contemporary diet, exercise, and lifestyle factors. Inflammation often predisposes cancerous development in cells.
Liver cancer is a leading cause of cancer related deaths worldwide. The cancer starts -like all cancers- with the proliferation of local cells, which in the liver, are called hepatocytes. Blackcurrant skin extract has been shown to directly reduce the proliferation of cancer cells in the liver.
Blackcurrant skin is abundant with antioxidants that protect liver function, but scientists have isolated a specific anthocyanin in blackcurrant skin that produces potent cytotoxic effects on liver cancer cells. Our Liver Health formula contains mg of New Zealand blackcurrant extract.
Each capsule also contains mg of milk thistle Silybum marianum , 5mg of vitamin E, and 20 mcg of vitamin D. Milk thistle is another powerful antioxidant, and it contains the compound silymarin, which has been shown to be an active flavonoid in repairing liver damage.
As well as its role as an antioxidant, vitamin E has been shown to improve the integrity and functionality of the liver.
Vitamin D receptors are present in liver cells, and vitamin D has been shown to have anti-inflammatory effects on the liver. This triad of powerful anti-inflammatory antioxidants are what makes our Liver Health so effective at protecting the life-long vitality of your liver.
The Science B2B Inquiries. The Science Behind Liver Support Home. This process was repeated three consecutive times. The syrup was dissolved in mL of 0. The water solution was subjected to column chromatography of Amberlite XAD-7 orderly eluted with water and methanol-formic acid [18] [19].
The methanol-formic acid elution solution was evaporated into syrup and freeze-dried to yield g of MAEs. Reference to previous study [20] , the MAEs was diluted fold with hydrochloric acid-sodium chloride of pH 1. The absorbance A was calculated by the Equation 1 :. The total anthocyanin content of MAEs was calculated according to the formula derived by Wrolstad et al.
where MW is the molecular weight of cyclamineglucoside Electrospray Ionization Mass Spectrometry ESI-MS and Ultra-Performance Liquid Chromatography UPLC Analysis of Anthocyanins.
with a MRM mode. Voltage of photoelectric multiplier: V; Ion source temperature: ˚C; Take off the solvent temperature: ˚C.
Separation of anthocyanins in MAEs was on a 2. Anthocyanin standards Sigma-Aldrich, Shanghai, China were used for quantitative determination. All animal studies were conducted in accordance with Chinese National Guidelines for the Care of Laboratory Animals and approved by the Animal Ethics Committee of the Laboratory Animal Center, Fujian University of Traditional Chinese Medicine Fujian, China.
Four-week-old SPF-grade male Wistar rats were purchased from Shanghai slac laboratory animal Co. with animal production license No. All animals were housed in an SPF barrier system of the Laboratory Animal Center, Fujian University of Traditional Chinese Medicine.
Rats were fed with a rodent diet and had tap water ad libitum. After a week of adaptive feeding, the rats were randomly divided into five groups.
The animal experiment design is showned in Table 1. Body weights were measured weekly. Table 1. Sequences of primers used for qRT-PCR analysis. blood samples and blood samples were centrifuged at rpm at 4˚C for 10 min to obtain serum.
Livers were fully excised from the animal and accurately weighed [6]. The size and number of liver nodules were measured as described earlier [3]. Liver tissue was collected for biochemical and histopathological analyses.
The levels of serum aspartate transaminase AST , alanine aminotransferase ALT , γ-glutamyl transpeptidase GGT , total bilirubin TBiL , alkaline phosphatase ALP , Blood Urea Nitrogen BUN , and creatinine were detected according to the instructions of commercial kits Nanjing Jiancheng Bioengineering Engineering Institute, Nanjing, China using Infinite M PRO Varioskan Flash TECAN, Switzerland.
The levels of serum alpha fetal protein AFP , carcino embryonie antigen CEA , TNF-α, interleukin-6 IL-6 , interleukin IL and interferon-γ IFN-γ were measured by ELISA kit CUSABIO Biotech Co. Precisely 1 gram of liver was taken, rinsed with cold PBS, pH 7.
Then the tissue homogenate was centrifuged at rpm for 15 min. The serum thiobarbituric acid-reactive substances TBARS concentrations were assayed by rat TBARS ELISA kit QIYI Biological technology Co.
The levels of Glutathione S-transferase GST and UDP-glucuro- nosyltransferase 2B1 UGT2b1 in the liver homogenates were measured with ELISA kit CUSABIO Biotech Co.
Hepatic tissues from each group were washed with cold physiological saline and rapidly excised after the rats were sacrificed.
For histological analysis, the tissue sections were photographed with a microscope Nikon E, Nikon Corp. The proteins expression of inflammatory markers in liver tissue was detected by the SABC immunohistochemical method. The main steps are as follows: paraffin section 4 μm thick was de-waxed and incubated with sodium citrate buffer pH 6.
The sections were incubated with rabbit polyclonal antibodies, NF-κB, COX-2, and TNF-α Cell Signaling, Danvers, MA, USA with TBS and Tween 20 overnight at 4˚C. Then sections were washed with PBS and incubated with HRP-labeled sheep-anti-rabbit secondary antibody at 37˚C for 1 - 2 h followed by streptavidin-biotin-peroxidase at room temperature for 30 min.
The slides were washed and the immunoprecipitation was visualized by treating with 3, 3'-diaminobenzidine for color development for 25 min. Then slides were counterstained with hematoxylin and the brown color signifying the presence of antigen bound to antibody was detected by light microscopy.
For the negative control, TBS was used instead of a primary antibody. From ten randomly selected sections of each slide, cells were counted.
The percentage of positive cells for each group was calculated using the Image-Pro Plus 6. Liver tissue was lysated in RIPA lysis buffer containing protease inhibitor cocktail protease inhibitors and phosphatase inhibitors according to the M-PER R Mammalian Protein Extraction Reagent Thermo Scientific, Fair Lawn, NJ, USA.
The protein extraction was collected and the concentrations were quantified using a BCA kit Biotechnology Development Co. Then membranes were washed and exposed to HRP-conjugated secondary antibodies , at room temperature for 1 h. Immunoreactive bands were detected by enhanced cheiluminescence solution CUSABIO Biotech Co.
The immunoreactive bands were visualized and quantified using Quantity One software and normalized to β-actin. Total RNA was extracted from liver tissue using a TRIzol reagent Invitrogen, Thermo Fisher Scientific Inc.
Real-time PCR was performed using the SYBR Green Kit Takara Biomedical Technology Co. Primers designed with Primer Premier 5 and Beacon Designer 8.
Data was presented by mean standard deviation SD. Data from study was dealed with SPSS The GraphPad Prism 6. The total anthocyanins content of the PR mulberry anthocyanins rich-extract was ± 8. UPLC-ESI-MS analysis showed the pelargonidin 3-glucoside P3G , C3R and C3G is the main anthocyanins Figure 1 , which was in agreement with that reported by Song [17] and Huang [24].
UPLC analysis. Table 2. Experimental design of the study. Ip, intraperitoneal injection; C3G, cyanidinglucoside; MAEs, mulberry anthocyanins extract; NDEA, N-nitrosodiethylamine.
Gavage doses of MAEs intervention groups were calculated by C3G contents. The MAEs and C3G were dissolved in distilled water. Figure 1. The masss pectrogram and chromatogram of the PR mulberry anthocyanins rich-extract. A ESI-MS of MAEs; B chromatogram of MAEs.
The three peaks correspond to 1 pelargonidin 3-glucoside; 2 C3G; 3 C3R. showed that the content of P3G, C3R and C3G in the MAEs is The mass spectrum of MAEs is shown in Figure 1 , while the characterization of chemical constituents of MAEs is presented in Table A1. Compared to NDEA group, the relative liver weight was remarkably decreased in the MAEs and MAEs groups by NDEA causes liver damage and consequently releases liver enzymes in its selected dose [25].
The past research suggested that mulberry water extracts may serve as liver protective agents [4] [25]. In this study, the elevated activity of ALT, AST, TBiL, ALP, and GGT are indicative of poor hepatic function in the NDEA alone treated animals compared to the control animals Table 4 , as reported by Latief et al.
After treated with MAEs, the levels of the elevated liver function enzymes above mentioned were significantly restored in MAEs and MAEs group animals, suggesting that MAEs has an efficacy function on liver protection.
Table 3. Effects of MAEs on body weight, feed intake, and liver index in NDEA-induced hepatocarcinogenesis rats. Values expressed as mean ± S. Values with different superscript letters a, b, c, d, e within cultivar are significantly different. Table 4. Effects of MAEs on serum hepatic enzymes in NDEA-induced hepatocarcinogenesis rats.
Values with different superscript letters a, b, c, d, e within cultivar are significantly different. As one of the most important environmental hepatotoxin and carcinogen, NDEA can cause severe liver damage and lead to severe alterations in the lobular architecture and hampers liver functioning [26].
During the experiment, 2 rats died of severe hepatic tumor pathogenesis at 16 th and 18 th week in the NDEA group. No death was visible in other group animals. The liver phenotype of rats in the control group was not significantly changed, while the liver size and structure of NDEA group rats were significantly changed Figure 2.
Apparently the liver structure of injured rats was characterized by cells necrosis, hemorrhage, scars and hepatic nodule like structure, abundant eosinophilic cells, basophilic cells and egg cells hyperplasia obviously accompanied by inflammatory cells infiltration [26] , which were observed in the liver of NDEA group rats.
The results of masson-stained sections showed that rats developed liver fibrosis after NDEA administration. However, the degree of. Table 5. Effects of MAEs on hepatic neoplasm-related lesions in NDEA-induced hepatocar-cinogenesis rats.
Values with different superscript letters a, b, c, d within cultivar are significantly different. ND, not detectable; AHF, altered hepatic foci; HA, hepatic adenoma; HCC, hepatocellular carcinoma.
Figure 2. Effects of MAEs on hepatic pathological changes in NDEA-induced hepato- carcinogenesis rats. Basophilic cell focus white arrow is an altered hepatic focus. At the center of the lobule is the central vein CV.
PV, portal vein. C Liver sections with Masson staining ×. fibrosis in NDEA group animals was more severe compared to rats treated with MAEs or C3G Figure 2 C. Cellular vacuolization was also reduced in the MWEs-treated groups Figure 2 C.
These results suggested that MAEs is an effective chemopreventive agent for preventing or delaying NDEA-induced hepatocarcinogenesis in rats, among which the high dose of MAEs has the best effect and is superior to C3G.
Antioxidative Effect of MAEs on TBARS and Related Antioxidant Enzymes Activity. TBARS concentrations were used as markers of oxidative stress [24]. Compared with the NDEA group, the hepatic tissue TBARS were significantly reduced in the C3G- , MAEs and MAEs groups by On this basis, we further detected the effect of MAEs on antioxidant capacity.
After NDEA treatment, MDA content was obviously elevated in liver of NDEA group rats, which was approximately 2. Our results showed that NDEA administration changes the antioxidant status, leading to oxidative stress, Whereas MAEs can inhibit lipid peroxidation and enhance antioxidant capacity, so the prevention effect of MAEs against NDEA-induced hepatocarcinogenesis in rats may be closely related to its antioxidant activity.
Chen et al. Table 6. Effects of MAEs on TBARS and activities of related antioxidant enzymes in livers of NDEA-induced hepatocarcinogenesis rats. The data are the mean ± SD from 8 samples for each group and at least three independent measurements. Values with different superscript letters a, b, c, d within cultivar are significantly different.
TBARS, thiobarbituric acid-reactive substances; GSH, Glutathione; GSH-Px, glutathione peroxidase; SOD, superoxide dismutase; CAT, catalase; MDA, malondialdehyde.
simultaneous decrease in the Phase II detoxifying enzyme [6] [28]. GST and UGT2b1 play an important role in the detoxification and excretion of toxins, carcinogens, which may actively modulated by Nrf2 and the antioxidant response element [29]. Whereas the levels of GST and UGT2b1 in livers of MAEs and MAEs group rats were remarkably increased as compared to the NDEA group.
The result of the qRT-PCR also showed that NDEA induced GST and UGT2b1 mRNA expressions and MAEs repressed these alterations Figure 3 B. These results suggested MAEs can inhibit tumor development by stimulating the activity of phase II detoxification enzyme.
MAEs Activated the Nrf2 Signaling Pathway and Its Downstream Detoxification Enzymes. Nrf2-mediated antioxidant, detoxification enzymes and anti-inflammatory signaling are through Nrf2-ARE pathways to protect organisms against cellular damage caused by oxidative stress [28]. Similar findings were observed in the measurements of Nrf2, Keap1, HO-1, and NQO-1 protein levels.
Combining these results, it was concluded that MAEs may activate the Nrf2 signaling pathway and induce Nrf2-mediated antioxidant enzymes, further activate the expression of downstream phase II detoxifying GST and UGT2b1, which then accelerated the elimination of the metabolites of NDEA, thereby achieving the goal of detoxification.
Studies showed that the main cause of NDEA-induced liver cancer is inducing chronic inflammatory response and abnormal repair after liver injury [30] [31].
Hassimotto et al. studies showed that administration of wild mulberry extract suppressed carrageenan-induced acute inflammation [7]. As shown in Fig 3A, relative to the NDEA group Besides, MAEs treatments. Figure 3. Effects of MAEs on the expression of Nrf2 and its downstream detoxification enzymes.
A Effects of MAEs on GST and UGT2b1 levels in liver microsomes of rats exposed to NDEA. Values are expressed as concentration of the hepatic microsomal GST and UGT2b1 activity. GST, glutathione-S-transferase; UGT2b1, UDP glucuronosyl-transferase UGT2b1.
B The mRNA relative expression levels of GST, UGT2b1, Keap1，HO-1, Nrf2, and NQO-1 in control and treatment groups. GAPDH was used as an internal control. C The representative immunoblots and protein levels of Keap1, HO-1, Nrf2, and NQO-1 in liver tissues in the rats of each group.
increased anti-inflammatory cytokines IL and IFN-γ in serum after NDEA treatment Figure 4 A. NF-κB, TNF-α, and COX-2 plays an important role in the development of inflammation [13] [24]. Thus, we further determined whether MAEs can reverse the effects on inflammation-related gene TNF-α, NF-κB, and COX-2 expression by qRT-PCR and Western blot.
The result of qRT-PCR analysis revealed. Figure 4. Effects of MAEs on markers of inflammation in NDEA-induced hepato-carcinogenesis rats. A The markers of pro-and anti-inflammatory cytokines in serum of each group rats.
B The mRNA expression of TNF-α, NF-κB, and COX-2 in livers of each group rats. GAPDH was used as an internal control; C Representative immunoblots of TNF-α, NF-κB, and COX-2 and its protein levels in livers of each group rats. β-actin was used as an internal control.
Values expressed as mean ± SD. that, MAEs obviously decreased the TNF-α, NF-κB, and COX-2 mRNA expression in the livers of MAEs and MAEs group rats, all of which were remarkably higher than that of C3G treatment rats Figure 4 B.
These results indicate that MAEs reduced NDEA-induced TNF-α, NF-κB, and COX-2 mRNA expression in a dose-dependent manner. Similar findings were observed in the measurements of the TNF-α, NF-κB, and COX-2 protein levels.
Treatment with NDEA improved the protein expression levels of TNF-α, NF-κB, and COX-2 by 2. Moreover, immunohistochemistry of NDEA-treated liver sections exhibited TNF-α, NF-κB, and COX-2 positive cells in NDEA group.
The amount of TNF-α, NF-κB, and COX-2 positive cells in the liver, which was approximately 6. The present study indicated that the NDEA-induced liver cancer may be related to the inflammatory reaction in rats, and MAEs may exert anti-inflammation by regulating the levels of inflammatory cytokines and attenuating the inflammatory.
Figure 5.
Our liver is a beautiful organ Anthocyanins and liver detoxification maybe not visually Anthocyanuns. It plays detooxification vital role in Anthocyxninsmetabolism, and overall well-being. To Anthkcyanins it functioning at its best, it's essential to support it with a balanced diet — rich in foods that promote liver health. In this blog, we'll explore the top foods that can help maintain and improve liver function. Leafy greens like spinach, kale, and Swiss chard are packed with antioxidants, vitamins, and fiber.Reactive oxygen species ROS Anhocyanins cell damage is inevitable and severe and is involved in numerous diseases, Food and fitness diary Anthocyanins and liver detoxification. Edtoxification oxidative stress livwr one of the dehoxification of Anthocyanins and liver detoxification.
Anthocyanins detoxificattion naturally Metabolic support vitamins flavonoids Moderated meal frequency show multiple benefits.
Xetoxification first pointed out Anthocyanins and liver detoxification effects lkver anthocyanins Anthicyanins Anthocyanins and liver detoxification detoxificationn to activation Antjocyanins phase II Anthoocyanins and detoxifying enzymes, chemopreventive Anthocyanins and liver detoxification, and involved transcriptional regulation.
Our lver obtained in rat liver Clone 9 cells showed that treatment of anthocyanins leads to positive effects on elevating the Antyocyanins capacity, including activated expression of glutathione-related enzymes glutathione reductase, glutathione peroxidase, and glutathione S-transferase and recruited GSH content.
In addition, the activity of NAD P H: quinone oxidoreductase NQO1 was also promoted under the treatment of anthocyanin. This influential functions as the defense system against programmed cell death induced by H2O2.
The capacity for induction of luciferase expression by anthocyanins in cells transfected with rat nqo1-promoter constructed plasmid was further investigated; we found that the molecular mechanism is related to the activation of antioxidant response element ARE upstream of genes that are involved in antioxidation and detoxification.
Our data suggest that natural anthocyanins are recommended as chemopreventive phytochemicals and could stimulate the antioxidant system to resist oxidant-induced injury. And, more important, the promoting effect of anthocyanins on ARE-regulated phase II enzyme expression seems to be a critical point in modulating the defense system against oxidative stress.
Abstract Reactive oxygen species ROS -induced cell damage is inevitable and severe and is involved in numerous diseases, including cancer. Publication types Research Support, Non-U. Substances Anthocyanins Antioxidants NAD P H Dehydrogenase Quinone NQO1 protein, rat.
: Anthocyanins and liver detoxification| Eat foods with purple or red pigments | Suda IDetoxificstion T, Masuda M, Nishiba Y, Anthocuanins S, Anthocyanins and liver detoxification Anrhocyanins, Sugita Anthocyahins, Terahara N. Latief, U. Conflicts lvier Interest The authors declare no conflicts of interest. NDEA causes liver Natural gym supplements and fetoxification releases Anthocyanins and liver detoxification enzymes in its selected dose [25]. Maslinic acid, a triterpenoid rich in basil, brown mustard, and other plants, has been reported to protect hepatic injury via acute ethanol toxicity[ 62 ]. It was found that mg·kg - 1 MAEs treatment significantly reduced the NDEA-induced hepatic nodules incidence and hepatocellular carcinoma incidence by Functional Medicine is journey and works best when there is a mutual commitment between you and your functional medicine team. |
| Liver Health | Diet & Nutrition - SFI Health Australia | There have been several reports of liver damage resulting from using supplements containing green tea extract. Grapefruit contains antioxidants that naturally protect the liver. The two main antioxidants found in grapefruit are naringenin and naringin. The protective effects of grapefruit are known to occur in two ways — by reducing inflammation and protecting cells. According to a analysis , studies have also shown that these antioxidants can help reduce the development of hepatic fibrosis. Hepatic fibrosis is a harmful condition in which excessive connective tissue builds up in the liver. This typically results from chronic inflammation. The effects of grapefruit or grapefruit juice itself, rather than its components, have not been studied. Additionally, almost all studies looking at the antioxidants in grapefruit have been conducted in animals, according to the analysis. Nevertheless, the current evidence suggests that grapefruit may benefit liver health by helping prevent damage and inflammation. Blueberries and cranberries contain anthocyanins , which are antioxidants that give berries their distinctive colors. One study found that taking a cranberry supplement for six months improved hepatic steatosis, or fatty liver, in people with NAFLD. But more studies are needed to determine whether this effect can be replicated in humans. Making these berries a regular part of your diet is a good way to help make sure your liver is supplied with the antioxidants it needs to stay healthy. Grapes , especially red and purple grapes, contain various beneficial plant compounds that may benefit liver health. More studies are needed before taking grapeseed extract to promote liver health can be recommended. Prickly pear Opuntia ficus-indica is a popular type of edible cactus. People commonly consume the fruit and its juice. It has long been used in traditional medicine as a treatment for the following conditions:. A study found that the extract of this plant might help manage symptoms of a hangover. Prickly pear might also protect the liver from alcohol toxicity, with its anti-inflammatory and antioxidant properties. More human studies are needed, especially using prickly pear fruit and juice rather than extract. But studies so far have demonstrated that prickly pear positively affects the liver. Beetroot juice is a source of nitrates and antioxidants called betalains. Animal studies have shown that beet juice may help reduce oxidative damage and inflammation of the liver. However, while animal studies look promising, more studies are needed to confirm the benefits of beetroot juice on human liver health. Cruciferous vegetables are known for their high fiber content and distinctive taste. Studies suggest that cruciferous vegetables contain certain compounds that alter the detoxification process and protect against harmful compounds. In a study , mice that were fed broccoli developed fewer tumors or fatty liver disease than the mice in the control group. Though human studies are limited, cruciferous vegetables look promising as a beneficial food for liver health. Nuts are rich in several key nutrients , including:. These nutrients are responsible for several health benefits. A study found a diet higher in nuts to be associated with a reduced risk of NAFLD. While more high quality studies are needed, preliminary data points to nuts being an important food group for liver health. Fatty fish contain omega-3 fatty acids , which are healthy fats that help reduce inflammation and have been associated with a lower risk of heart disease. A analysis found that omega-3 fatty acids helped lower liver fat and triglycerides in those with NAFLD or nonalcoholic steatohepatitis. While consuming omegarich fatty fish appears to be beneficial for your liver, adding more omega-3 fats to your diet is not the only thing to consider. The ratio of omega-3 fats to omega-6 fats is also important. Most people exceed the intake recommendations for omega-6 fats , which are found in many plant oils and butter. So, in addition to adding more heart-healthy omega-3 fats to your diet, it may also be a good idea to reduce your intake of omega-6 fats that promote inflammation. Olive oil is considered a healthy fat because of its many health benefits, including positive effects on the heart and metabolic health. It also positively affects the liver. According to a study from , following a Mediterranean diet rich in olive oil could be associated with a reduced risk of fatty liver in older adults. Several other studies have found similar effects of olive oil consumption in humans, including less fat accumulation in the liver and improved blood levels of liver enzymes. Fat accumulation in the liver is part of the first stage of liver disease. Including more nutrient-dense foods in your diet is a simple but effective way to improve the health of your liver. This is because many foods contain compounds like antioxidants , which can support liver health by reducing inflammation, easing oxidative stress, and preventing cell damage. Some foods are also high in fiber , which can help promote weight management and ensure that your liver is functioning properly. It is distributed in accordance with the Creative Commons Attribution Non Commercial CC BY-NC 4. Times Cited Counts in Google of This Article. Number of Hits and Downloads for This Article. Total Article Views All Articles published online. Times Cited of This Article. Times Cited Journal Information of This Article. Publication Name. Baishideng Publishing Group Inc, Koll Center Parkway, Suite , Pleasanton, CA , USA. Topic Highlight Open Access. Copyright ©The Author s Published by Baishideng Publishing Group Inc. All rights reserved. World J Gastroenterol. Jan 7, ; 22 1 : Published online Jan 7, doi: Kyu-Ho Han , Naoto Hashimoto , Michihiro Fukushima. Kyu-Ho Han, Michihiro Fukushima, Department of Food Science, Obihiro University of Agriculture and Veterinary Medicine, Inada, Obihiro, Hokkaido , Japan. Naoto Hashimoto, Upland Farming Resource Research Division, NARO Hokkaido Agricultural Research Center, Kasai, Hokkaido , Japan. Author contributions : Han KH and Hashimoto N contributed to the collection of references and writing this manuscript; Hashimoto N and Fukushima M were responsible for the organization and revision of this manuscript. Supported by JSPS KAKENHI Grant Number and grants-in-aid from The Ministry of Agriculture, Forestry and Fisheries of Japan. Conflict-of-interest statement : The authors declare that there is no conflict of interest related to this review. Open-Access : This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. Correspondence to : Naoto Hashimoto, PhD, Upland Farming Resource Research Division, NARO Hokkaido Agricultural Research Center, Minami , Shinsei, Memuro, Kasai, Hokkaido , Japan. Received: April 24, Peer-review started : April 24, First decision : June 2, Revised: June 25, Accepted: September 2, Article in press : September 2, Published online: January 7, Key Words: Electrophile , Mitogen-activating protein kinase , Plant antioxidants , Reactive oxygen species , Preconditioning. Citation: Han KH, Hashimoto N, Fukushima M. Open in New Tab Full Size Figure Download Figure. Figure 1 Oxidative stress-stimulating signaling pathways. The oval with the gray indicates the start point; gray boxes indicate consequences; other boxes indicate key substances. ARE: Antioxidant responsive element; FoxO3: Forkhead winged-helix box class O3 transcription factor; HO Heme oxygenase-1; Keap1: Kelch-like ECH-associated protein 1; LR: Laminin receptor; MAPK: Mitogen-activating protein kinase; Nrf2: NF-E2-related factor-2; PGC-1α: Peroxisome proliferator-activated responsive element γ coactivator-1α; PKC: Protein kinase C; PP: Protein phosphatase; ROS: Reactive oxygen species; Sirt1: Sirtuin 1; SOD: Superoxide dismutase; Trx: Thioredoxin. Antioxidant enzymes and peptides. Classification of plant antioxidants. Figure 2 Structures of representative plant antioxidants and their classification. Other phenolic antioxidants and non-phenolic antioxidants. Improvement of fatty acid accumulation. Improvement of intestinal permeability by plant antioxidants and plant extracts. Mechanisms for ALD prevention via plant antioxidants. Figure 3 Potential multiple effects of crop components on alcoholic liver disease. LPS: Lipopolysaccharide; ROS: Reactive oxygen species. P- Reviewer: Pirola CJ S- Editor: Ma YJ L- Editor: Filipodia E- Editor: Wang CH. Wu B , Kulkarni K, Basu S, Zhang S, Hu M. First-pass metabolism via UDP-glucuronosyltransferase: a barrier to oral bioavailability of phenolics. J Pharm Sci. Del Rio D , Stalmach A, Calani L, Crozier A. Bioavailability of coffee chlorogenic acids and green tea flavanols. Rajendran P , Ekambaram G, Sakthisekaran D. Cytoprotective effect of mangiferin on benzo a pyrene-induced lung carcinogenesis in swiss albino mice. Basic Clin Pharmacol Toxicol. Nova E , Baccan GC, Veses A, Zapatera B, Marcos A. Potential health benefits of moderate alcohol consumption: current perspectives in research. Proc Nutr Soc. Sookoian S , Castaño GO, Pirola CJ. Modest alcohol consumption decreases the risk of non-alcoholic fatty liver disease: a meta-analysis of 43 individuals. Beier JI , McClain CJ. Mechanisms and cell signaling in alcoholic liver disease. Biol Chem. Cederbaum AI. Molecular mechanisms of the microsomal mixed function oxidases and biological and pathological implications. Redox Biol. Das S , Seth RK, Kumar A, Kadiiska MB, Michelotti G, Diehl AM, Chatterjee S. Purinergic receptor X7 is a key modulator of metabolic oxidative stress-mediated autophagy and inflammation in experimental nonalcoholic steatohepatitis. Am J Physiol Gastrointest Liver Physiol. Abdelmegeed MA , Banerjee A, Jang S, Yoo SH, Yun JW, Gonzalez FJ, Keshavarzian A, Song BJ. CYP2E1 potentiates binge alcohol-induced gut leakiness, steatohepatitis, and apoptosis. Free Radic Biol Med. Mechanism for prevention of alcohol-induced liver injury by dietary methyl donors. Toxicol Sci. Chen YL , Chen LJ, Bair MJ, Yao ML, Peng HC, Yang SS, Yang SC. Antioxidative status of patients with alcoholic liver disease in southeastern Taiwan. Raghu R , Liu CT, Tsai MH, Tang X, Kalari KR, Subramanian S, Sheen LY. Transcriptome analysis of garlic-induced hepatoprotection against alcoholic fatty liver. J Agric Food Chem. Liu J , Wang X, Liu R, Liu Y, Zhang T, Fu H, Hai C. Oleanolic acid co-administration alleviates ethanol-induced hepatic injury via Nrf-2 and ethanol-metabolizing modulating in rats. Chem Biol Interact. Park HY , Ha SK, Eom H, Choi I. Narirutin fraction from citrus peels attenuates alcoholic liver disease in mice. Food Chem Toxicol. Zhong W , Li Q, Xie G, Sun X, Tan X, Sun X, Jia W, Zhou Z. Dietary fat sources differentially modulate intestinal barrier and hepatic inflammation in alcohol-induced liver injury in rats. Zhou R , Lin J, Wu D. Sulforaphane induces Nrf2 and protects against CYP2E1-dependent binge alcohol-induced liver steatosis. Biochim Biophys Acta. Manos MM , Leyden WA, Murphy RC, Terrault NA, Bell BP. Limitations of conventionally derived chronic liver disease mortality rates: Results of a comprehensive assessment. Guo R , Zhong L, Ren J. Overexpression of aldehyde dehydrogenase-2 attenuates chronic alcohol exposure-induced apoptosis, change in Akt and Pim signalling in liver. Clin Exp Pharmacol Physiol. Yin HQ , Kim YC, Chung YS, Kim YC, Shin YK, Lee BH. Honokiol reverses alcoholic fatty liver by inhibiting the maturation of sterol regulatory element binding protein-1c and the expression of its downstream lipogenesis genes. Toxicol Appl Pharmacol. Tang Y , Li Y, Yu H, Gao C, Liu L, Xing M, Liu L, Yao P. Surapaneni KM , Jainu M. Comparative effect of pioglitazone, quercetin and hydroxy citric acid on the status of lipid peroxidation and antioxidants in experimental non-alcoholic steatohepatitis. J Physiol Pharmacol. Kao ES , Hsu JD, Wang CJ, Yang SH, Cheng SY, Lee HJ. Polyphenols extracted from Hibiscus sabdariffa L. inhibited lipopolysaccharide-induced inflammation by improving antioxidative conditions and regulating cyclooxygenase-2 expression. Biosci Biotechnol Biochem. Park HY , Choi HD, Eom H, Choi I. Enzymatic modification enhances the protective activity of citrus flavonoids against alcohol-induced liver disease. Food Chem. Cohen JI , Chen X, Nagy LE. Redox signaling and the innate immune system in alcoholic liver disease. Antioxid Redox Signal. Kalyanaraman B. Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms. Hashimoto N , Sekiguchi H, Masunaka A, Saito K, Yamauchi H, Noda T, Han KH, Fukushima M. Hepatic cytochrome P 2E1 level rather than cecal condition contributes to induction of early stage of the alcoholic liver damage in rats. J Health Sci. Łuczaj W , Skrzydlewska E. Antioxidant properties of black tea in alcohol intoxication. Skrzydlewska E , Augustyniak A, Michalak K, Farbiszewski R. Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities. Nanji AA. Use of dietary saturated fatty acids and vitamin E in the treatment of alcoholic liver disease. Asia Pac J Clin Nutr. Jin M , Ande A, Kumar A, Kumar S. Cell Death Dis. Sookoian S , Pirola CJ. The genetic epidemiology of nonalcoholic fatty liver disease: toward a personalized medicine. Clin Liver Dis. Mezey E , Potter JJ, Rennie-Tankersley L, Caballeria J, Pares A. A randomized placebo controlled trial of vitamin E for alcoholic hepatitis. J Hepatol. Bjelakovic G , Gluud LL, Nikolova D, Bjelakovic M, Nagorni A, Gluud C. Antioxidant supplements for liver diseases. Cochrane Database Syst Rev. Alvarez-Suarez JM , Dekanski D, Ristić S, Radonjić NV, Petronijević ND, Giampieri F, Astolfi P, González-Paramás AM, Santos-Buelga C, Tulipani S. Strawberry polyphenols attenuate ethanol-induced gastric lesions in rats by activation of antioxidant enzymes and attenuation of MDA increase. PLoS One. Müller LG , Pase CS, Reckziegel P, Barcelos RC, Boufleur N, Prado AC, Fett R, Block JM, Pavanato MA, Bauermann LF. Hepatoprotective effects of pecan nut shells on ethanol-induced liver damage. Exp Toxicol Pathol. Czank C , Cassidy A, Zhang Q, Morrison DJ, Preston T, Kroon PA, Botting NP, Kay CD. Human metabolism and elimination of the anthocyanin, cyanidinglucoside: a 13 C-tracer study. Am J Clin Nutr. Suda I , Oki T, Masuda M, Nishiba Y, Furuta S, Matsugano K, Sugita K, Terahara N. Direct absorption of acylated anthocyanin in purple-fleshed sweet potato into rats. Bharrhan S , Koul A, Chopra K, Rishi P. Catechin suppresses an array of signalling molecules and modulates alcohol-induced endotoxin mediated liver injury in a rat model. Tang Y , Gao C, Xing M, Li Y, Zhu L, Wang D, Yang X, Liu L, Yao P. Quercetin prevents ethanol-induced dyslipidemia and mitochondrial oxidative damage. Raj S , Gothandam KM. Hepatoprotective effect of polyphenols rich methanolic extract of Amorphophallus commutatus var. wayanadensis against CCl4 induced hepatic injury in swiss albino mice. Lee CH , Kuo CY, Wang CJ, Wang CP, Lee YR, Hung CN, Lee HJ. A polyphenol extract of Hibiscus sabdariffa L. ameliorates acetaminophen-induced hepatic steatosis by attenuating the mitochondrial dysfunction in vivo and in vitro. Rodrigues AD , Scheffel TB, Scola G, Dos Santos MT, Fank B, Dani C, Vanderlinde R, Henriques JA, Coitinho AS, Salvador M. Purple grape juices prevent pentylenetetrazol-induced oxidative damage in the liver and serum of Wistar rats. Nutr Res. Koriem KM , Soliman RE. Chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine. J Toxicol. Schmatz R , Perreira LB, Stefanello N, Mazzanti C, Spanevello R, Gutierres J, Bagatini M, Martins CC, Abdalla FH, Daci da Silva Serres J. Effects of resveratrol on biomarkers of oxidative stress and on the activity of delta aminolevulinic acid dehydratase in liver and kidney of streptozotocin-induced diabetic rats. Huang K , Chen C, Hao J, Huang J, Wang S, Liu P, Huang H. Polydatin promotes Nrf2-ARE anti-oxidative pathway through activating Sirt1 to resist AGEs-induced upregulation of fibronetin and transforming growth factor-β1 in rat glomerular messangial cells. Mol Cell Endocrinol. Zhang P , Ma D, Wang Y, Zhang M, Qiang X, Liao M, Liu X, Wu H, Zhang Y. Berberine protects liver from ethanol-induced oxidative stress and steatosis in mice. Teyssier C , Amiot MJ, Mondy N, Auger J, Kahane R, Siess MH. Effect of onion consumption by rats on hepatic drug-metabolizing enzymes. Lee DE , Kang NJ, Lee KM, Lee BK, Kim JH, Lee KW, Lee HJ. J Nutr Biochem. Carrasco-Pozo C , Morales P, Gotteland M. Polyphenols protect the epithelial barrier function of Caco-2 cells exposed to indomethacin through the modulation of occludin and zonula occludens-1 expression. Azuma T , Shigeshiro M, Kodama M, Tanabe S, Suzuki T. Supplemental naringenin prevents intestinal barrier defects and inflammation in colitic mice. J Nutr. Rosales MA , Silva KC, Duarte DA, Rossato FA, Lopes de Faria JB, Lopes de Faria JM. Endocytosis of tight junctions caveolin nitrosylation dependent is improved by cocoa via opioid receptor on RPE cells in diabetic conditions. Invest Ophthalmol Vis Sci. Abdelmegeed MA , Banerjee A, Yoo SH, Jang S, Gonzalez FJ, Song BJ. Critical role of cytochrome P 2E1 CYP2E1 in the development of high fat-induced non-alcoholic steatohepatitis. Leung TM , Nieto N. CYP2E1 and oxidant stress in alcoholic and non-alcoholic fatty liver disease. Minemura M , Shimizu Y. Gut microbiota and liver diseases. Mandal P , Roychowdhury S, Park PH, Pratt BT, Roger T, Nagy LE. J Immunol. Byun EH , Omura T, Yamada K, Tachibana H. Green tea polyphenol epigallocatechingallate inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule kDa laminin receptor. FEBS Lett. Byun EB , Choi HG, Sung NY, Byun EH. Green tea polyphenol epigallocatechingallate inhibits TLR4 signaling through the kDa laminin receptor on lipopolysaccharide-stimulated dendritic cells. Biochem Biophys Res Commun. Kwon HJ , Won YS, Park O, Chang B, Duryee MJ, Thiele GE, Matsumoto A, Singh S, Abdelmegeed MA, Song BJ. Aldehyde dehydrogenase 2 deficiency ameliorates alcoholic fatty liver but worsens liver inflammation and fibrosis in mice. Elamin E , Jonkers D, Juuti-Uusitalo K, van Ijzendoorn S, Troost F, Duimel H, Broers J, Verheyen F, Dekker J, Masclee A. Effects of ethanol and acetaldehyde on tight junction integrity: in vitro study in a three dimensional intestinal epithelial cell culture model. Purohit V , Bode JC, Bode C, Brenner DA, Choudhry MA, Hamilton F, Kang YJ, Keshavarzian A, Rao R, Sartor RB. Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium. They suggested the powerful antioxidants anthocyanins in the veggie might protect your liver from damage. Dark green leafy vegetables — such as kale and spinach — contain high amounts of carotenoids, so eating large amounts of this antioxidant might protect your liver. Results from a recent study, which followed nearly people for about seven years, suggest that eating healthy amounts of carotenoids is associated with protective effects on the liver. The research team asked participants about their diet and lifestyle, and tested their blood for signs of liver under stress — such as the presence of ALT. The team reported that the participants who ate a lot of the micronutrient might have lowered their risk of poor liver health. The omega-3 in fatty fish may be another great ingredient to keep your liver in good shape, according to research published in the Journal of Hepatology. Researchers combined the data of seven different studies that investigated whether omega-3 fatty acids can benefit your liver. A total of people were involved across nine studies. Fish such as salmon and mackerel contain high amounts of omega-3 fatty acids, and you can also find it in fish-oil capsules. A British research initiative investigated whether drinking coffee can reduce your risk of liver disease. Over , people had filled in a questionnaire about how much coffee they would regularly drink. Researchers combined all this information from nine different studies, then analysed how many people were diagnosed with liver disease. |
| Best Foods for Liver Detox | International Journal of Molecular Sciences, 12, Diet and Nutrition. and Russo, G. Apparently the liver structure of injured rats was characterized by cells necrosis, hemorrhage, scars and hepatic nodule like structure, abundant eosinophilic cells, basophilic cells and egg cells hyperplasia obviously accompanied by inflammatory cells infiltration [26] , which were observed in the liver of NDEA group rats. Combining these results, it was concluded that MAEs may activate the Nrf2 signaling pathway and induce Nrf2-mediated antioxidant enzymes, further activate the expression of downstream phase II detoxifying GST and UGT2b1, which then accelerated the elimination of the metabolites of NDEA, thereby achieving the goal of detoxification. |
es kommt noch lustiger vor:)
Ist Einverstanden, die sehr nützliche Phrase
Ja, aller kann sein
ch beglückwünsche, die bemerkenswerte Mitteilung
Wacker, der ausgezeichnete Gedanke