Quercetin and arthritis -
QG is a dietary supplement in the flavonoid class found in many foods including black and green tea, apples, red onions, grapes, green leafy vegetables, and berries to name a few.
Several properties have been suggested for QGs including anti-viral, glucose stabilization, anti-cancer, and anti-inflammation. One animal study found that it and other flavones helped to stabilize cartilage breakdown by suppressing the cartilage breakdown pathways.
I was only able to find one other human study in arthritis, but in that study the same combination glucosamine-chondroitin-quercetin helped reduce pain and increase function in osteoarthritis patients but not rheumatoid arthritis patients.
The supplements seemed to work by improving the properties of the synovial fluid in the knee. The upshot? IMHO, the data on glucosamine and chondroitin is solid enough that these important dietary supplements should be taken by every arthritis patient.
While Quercetin has a strange name, the emerging data on combining QGs with glucosamine and chondoitin looks very promising.
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More Evidence Glucosamine and Chondroitin Work: What the Heck is Quercetin? Its overexpression results in a failure in joint formation, hypertrophy of skeletal elements, and excessive proliferation of epiphyseal cartilage [8, 57 , 58 ].
On the other hand, decreased GDF5 expression is linked with the degradation of chondrocyte ECM [ 59 ]. Other findings have shown that genes related to GDF5 , such as OPG, RANKL, and collagen type II genes, are involved in this pathologic condition Fig.
These genes cause irregular bone remodeling and decreased mineralization in an abnormal state [ 60 ]. OA and its pathogenic mechanisms.
IL, interleukin; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; TNF-α, tumor necrosis factor-α; MMPs, matrix metalloproteinases; NGF , nerve growth factor; GDF5 , growth differentiation factor 5; OPG, osteoprotegerin; RANKL, receptor activator of nuclear factor kappa-B ligand; SASP, senescence-associated secretory phenotype.
Que, as one of the six subclasses of flavonoid compounds, and its derivations are used in many industries, such as the medical and food industries [ 61 ]. In medical industries, Que can exert health-promoting effects in different human and animal cellular models because of its antioxidant and anti-inflammatory [ 61 ], antimicrobial [ 62 ], anticancer [ 63 ], wound healing [ 64 ], antiallergic [ 65 ], and antidiabetic effects [ 66 ].
Furthermore, Que can be a suitable candidate to fight against viral agents like severe acute respiratory syndrome coronavirus 2 [ 67 ], cardiovascular diseases [ 68 ], and autoimmune disorders [ 69 ]. Despite these, using Que has some pharmacological limitations, for example, very low solubility in water and high instability in the heat, light, and air [ 71 ].
Also, Que bioavailability, defined as the first administered dose that reaches the systemic circulation, is minimum because of its mass metabolism; thereby, its high dosage administration is needed [ 61 ].
Fortunately, modification processes can improve these problems [ 72 ]. These processes are divided into two types; either a derivation of Que or recombination with other active groups. The first type alters the structure of Que and enhances its solubility through derivation, whereas the second exerts a synergistic effect with the help of active groups, for instance, metal ions and complex ions; thus, the pharmacological action and bioactivity of Que can considerably be improved [ 72 ].
As a result, it seems that Que is a potential option for many medical purposes, and its curative influences can be increased by using the strategies that improve its bioavailability and solubility properties. Many in vitro and in vivo studies have focused on the therapeutic effects of Que on joint related-disorders, especially OA [ ].
In preclinical studies of OA, rheumatoid arthritis RA , and gouty arthritis, Que has revealed significant antiarthritic properties and joint protective effects [ 73 ].
This natural compound has protective impacts on articular cartilage by interfering with the p38 MAPK pathway [ 76 ]. MAPK is a signaling protein related to OA that has a critical role in monitoring the function of pathways modulating the formation and activity of factors of joint tissue damage [ 76, 77 ].
Que can also be effective in OA prevention and treatment by regulating the expression of inflammatory factors by blocking the p38 MAPK signaling pathway [ 78 ].
In an experimental work, the importance of suppression of inflammatory mediators in OA amelioration was highlighted. Similarly, Li et al. Moreover, another study investigated the immunomodulatory impact of Que on OA in vivo and in vitro , and it was concluded that Que makes a pro-chondrogenic circumstance and potentiates cartilage repair through the regulation of polarization of synovial macrophages to M 2 macrophages [ 74 ].
Also, an investigation in studied the effects of Que in animal models of surgical-induced OA. In this work, Que upregulated tissue inhibitor of metalloproteinases-1 and superoxide dismutase expressions, attenuated MMP expression, and improved OA degeneration by decreasing oxidative stress and curbing the degradation of ECM of the cartilage [ 80 ].
In Table 1 , therapeutic capacity of Que in treating OA has been summarized. On the whole, it seems that Que can be a desired candidate for OA treatment through various mechanisms, like improving the antioxidant system, regulating immune system reactions, and affecting signaling pathways related to joint and cartilage repair.
Que and its biologic and pharmacologic mechanisms for OA treatment. SOD, superoxide dismutase; ECM, extracellular matrix; TLR-4, Toll-like receptor 4; IRAK1, interleukin-1 receptor associated kinase 1; NLRP3, NLR family pyrin domain containing 3; Nrf2, nuclear factor erythroid 2-related factor; HO-1, heme oxygenase-1; COX-2, cyclooxygenase Many clinical trials have been carried out to evaluate Que effects on many systematic and regional disorders, like RA [ 82 ], OA [ 83 ], and many other diseases [ ].
For example, Kanzaki et al. This project implicated that this supplement could improve symptoms related to OA according to the Japanese Orthopedic Association criteria [ 83 ]. In another clinical work, a supplement containing Que glucoside, chondroitin, and glucosamine, was prescribed orally in patients with OA and RA.
This study demonstrated that the supplement could dramatically ameliorate pain symptoms, visual analog scale, and daily activities in OA cases. However, these impacts were not found in RA cases. In addition, they observed a remark reduction in the level of chondroitin 4-sulfate, which is formed through injured articular cartilage [ 88 ].
Javadi et al. Based on this research, Que consumption for 8 weeks diminishes early morning stiffness and pain considerably. Plus, the high-sensitivity TNF-α plasma level was remarkably reduced [ 82 ].
However, one clinical study showed that Que had no impact on blood pressure and inflammatory and oxidative situation of RA subjects [ 89 ]. It looks like the curative influences of Que need to be more evaluated in clinical studies.
OA, as one of the debilitating diseases, involves a great number of subjects worldwide and is linked with serious conditions that may be threatening life, like cardiovascular diseases, metabolic syndrome, and autoimmune diseases.
Among this, treatment with natural supplements, especially Que, has gained considerable attention due to its fewer side effects and high effectiveness. It has been indicated that Que can be a novel candidate against OA through various mechanisms, like modification of inflammatory agents, such as IL-1β, TNF-α, IL-6, and IL, inhibition of oxidative stress, ECM degeneration of the cartilage, and decrease of chondroitin 4-sulfate level; however, more experimental and clinical investigations are demanded to approve its effectiveness for OA treatment.
Faezeh Samadi contributed to the write-up of the review article. Mohammad Saeed Kahrizi, Fateme Heydari, Hossein Roghani-Shahraki, Abnoos Mokhtari Ardekani, and Fatemeh Rezaei-Tazangi designed the framework of the manuscript. Reza ArefNezhad contributed to the acquisition, analysis, and interpretation of data for the work.
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OA and Its Pathogenesis. Que: Therapeutic Benefits and Challenges. Que and OA. Que and Clinical Trials. Conflict of Interest Statement. Funding Sources. Author Contributions. Article Navigation. Review Articles July 06 Quercetin and Osteoarthritis: A Mechanistic Review on the Present Documents Subject Area: Pharmacology.
Faezeh Samadi ; Faezeh Samadi. a School of Nursing and Midwifery, Tehran University of Medical Science, Tehran, Iran. This Site. Google Scholar. Mohammad Saeed Kahrizi ; Mohammad Saeed Kahrizi.
b Department of Surgery, Alborz University of Medical Sciences, Karaj, Iran. Fateme Heydari ; Fateme Heydari. c Student Research Committee, School of Medicine, Shahid Beheshti of Medical Sciences, Tehran, Iran.
Reza Arefnezhad ; Reza Arefnezhad. d Department of Anatomy, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Hossein Roghani-Shahraki Hossein Roghani-Shahraki. e Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Abnoos Mokhtari Ardekani ; Abnoos Mokhtari Ardekani. f Endocrinology and Metabolism Research Center, Physiology Research Center, Institute of Basic and Clinical Physiology Science, Kerman University of Medical Sciences, Kerman, Iran.
Fatemeh Rezaei-Tazangi Fatemeh Rezaei-Tazangi. g Department of Anatomy, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran. rezaei67 yahoo. Pharmacology : — Article history Received:. Cite Icon Cite. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest.
View large Download slide. Table 1. View large. View Large. The figures were created by the web-based software BioRender.
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Editors-in-Chief: Andras Guttman Research Institute of Athritis and Quercetin and arthritis Engineering University Enhancing nutrient absorption Pannonia Veszprém Hungary. ISSN Print : ISSN Arthfitis : Abd DOI: arrthritis Diet plays a significant role in ensuring healthy life, and the bioactive compounds present in food and medicinal plants may be developed as drugs that combat various illnesses. A bioactive flavanoid, quercetin which is a dietary component, possesses numerous health-promoting effects. In preclinical models of rheumatoid arthritis, gouty arthritis and osteoarthritis, quercetin has shown significant joint protective effects. Autoimmune arthritiis are Arthrifis worldwide health problem with arthritiss rates Gluten-free breakfast options morbidity, and are characterized by breakdown and dysregulation of Quercetin and arthritis immune Quercetln. Although their etiology and Iron in ancient civilizations remain unclear, the application of dietary supplements Qufrcetin gradually increasing arthhritis patients with autoimmune znd, mainly due to their positive effects, Quercdtin safety, and Quercetin and arthritis cost. Quercetin is a natural flavonoid that is widely present in fruits, herbs, and vegetables. It has been shown to have a wide range of beneficial effects and biological activities, including anti-inflammation, anti-oxidation, and neuroprotection. In several recent studies quercetin has reportedly attenuated rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and systemic lupus erythematosus in humans or animal models. This review summarizes the evidence for the pharmacological application of quercetin for autoimmune diseases, which supports the view that quercetin may be useful for their prevention and treatment. Autoimmune diseases are a heterogeneous cluster of disorders characterized by systemic syndromes, in which autoreactive adaptive immune responses contribute to immune-mediated damage to cells and organs 1.
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