Quercetin and memory enhancement -
They also completed annual cognitive and memory tests including recalling lists of words, remembering numbers and putting them in the correct order. They were also asked about other factors, such as their level of education, how much time they spent doing physical activities and how much time they spent doing mentally engaging activities such as reading and playing games.
They were followed for an average of seven years. The people were divided into five equal groups based on the amount of flavonols they had in their diet. While the average amount of flavonol intake in US adults is about 16 to 20 milligrams mg per day, the study population had an average dietary intake of total flavonols of approximately 10 mg per day.
The lowest group had an intake of about 5 mg per day and the highest group consumed an average of 15 mg per day; which is equivalent to about one cup of dark leafy greens.
To determine rates of cognitive decline, researchers used an overall global cognition score summarizing 19 cognitive tests. The average score ranged from 0. After adjusting for other factors that could affect the rate of memory decline, such as age, sex and smoking, researchers found that the cognitive score of people who had the highest intake of flavonols declined at a rate of 0.
Holland noted this is probably due to the inherent antioxidant and anti-inflammatory properties of flavonols. The study also broke the flavonol class down into the four constituents: kaempferol, quercetin, myricetin and isorhamnetin.
The top food contributors for each category were: kale, beans, tea, spinach and broccoli for kaempferol; tomatoes, kale, apples and tea for quercetin; tea, wine, kale, oranges and tomatoes for myricetin; and pears, olive oil, wine and tomato sauce for isorhamnetin.
People who had the highest intake of kaempferol had a 0. Those with the highest intake of quercetin had a 0. And people with the highest intake of myricetin had a 0.
The 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide MTT was purchased from Bachem Bubendorf, Switzerland. Dimethyl sulfoxide and other common chemicals were obtained from Sigma-Aldrich Merck Millipore.
The PC12 rat pheochromocytoma cell line was purchased from the Japanese Collection of Research Bioresources Shinjuku, Japan. The cells were cultured in minimum essential medium Gibco; Thermo Fisher Scientific, Inc.
The ability of a compound to interact with the stable DPPH free radical indicates its capacity to quench free radicals. Quercetin treatment exhibits antiradical activity by inhibiting DPPH radicals. For investigating the radical scavenging activities, 10 mM quercetin in methyl alcohol was further diluted using methyl alcohol to obtain 5, 10, 20, 50 and µM solutions.
To each of the solutions of quercetin, 0. was added, followed by incubation for 45 min at room temperature. The optical density of each of the solutions was then measured using a spectrophotometer at nm. The control used was pure ethyl alcohol and its absorbance was denoted as A0, whereas the absorbance of the sample solution was denoted asAq.
The effects on cell viability and the neuroprotective effect exhibited by quercetin were determined using an MTT assay. For this purpose, cells at a density of 2× cells per well were distributed onto well plates and cultured overnight.
The media were then removed and the cells were exposed to either saline as a control, selegiline 10 µM as a positive control or different quercetin 10— µM and incubated for 48 h at 37°C.
Following incubation, MTT solution was added to each of the wells and the plates were incubated for 2 h at 37°C. Dimethyl sulfoxide was added to the wells for dissolution of the formazan crystals, which had formed. A microplate reader Model ; Bio-Rad Laboratories, Inc. For each of the analyses, three replicate wells were used.
The mice were acclimatized to the laboratory environment 1 week prior to commencement of the experiments, and were housed in a room with a 12 h light and dark cycle at a temperature of 25°C. The animals had access to standard food and water ad libitum.
All animal experimental procedures were performed following approval from the Laboratory Animal Care Committee of Sichuan Province Sichuan, China. For determination of the role of quercetin on spatial working memory following 4 days of Aβ injections, a Y-maze test was performed.
The instrument consisted of a maze, which was 35 cm in length, 16 cm in height and 12 cm in width. The instrument has arms, which are projected symmetrically.
The mice were placed in one of the arms and allowed to enter the other arms for 10 min. The determination of the role of quercetin on learning and memory following 6 days of Aβ injection was performed using a passive avoidance test.
The instrument consists of a double compartment step-through passive avoidance apparatus Model PACS; Columbus Instruments International, Columbus, OH, USA. Internally, the instrument had two similar chambers 24×16×16 cm.
One of the chambers contained a bulb for lighting, whereas the second chamber was covered with black film. The mice from the lit chamber were allowed to enter the dark chamber by the raising of a door, where they received a 1 sec foot shock during the training period.
Training consisted of two 5-day sessions, with 4 trials per session. The intersession gap was 2 h and inter-trial gap was 30 sec. Following the completion of training, the latency period taken to enter the dark chamber for each mouse was recorded.
To determine the acute oral toxicity induced by quercetin treatment in the mice, a lethality assay was used. Briefly, the mice were divided into five groups of five mice. The mice in the control group received normal saline and carboxymethyl cellulose CMC. The animals were examined following the administration of the doses for h.
All data are presented as the mean ± standard error of the mean. Student's t-test was used for statistical comparisons. All statistical tests were calculated using SPSS The primary factor examined in determining the anti-oxidant nature of a compound is its scavenging activity for oxygen radicals The results revealed that quercetin was potentially involved in the inhibition of DPPH radical activity.
It reduced the radical activity of DPPH by To investigate the effect of quercetin on the viability of PC12 cells, an MTT assay was used. The results showed that treatment of the PC12 cells with different concentrations of quercetin for 24 h induce no toxicity Fig.
Quercetin treatment has no significant effect on the viability of PC12 cells. PC12 cells were exposed to different concentrations of quercetin for 24 h and cell viability was examined using a 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide assay.
The data is presented as the mean percentage of viable cells. For investigating the effect of quercetin on the reduced viability of PC12 cells induced by Aβtreatment, an MTT assay was used.
The PC12 cells were exposed to a range of quercetin concentrations 10— µM prior to incubation with Aβ. The results revealed that pretreatment of the PC12 cells with quercetin inhibited the decrease in cell viability induced by Aβ Fig. Pretreatment of the cells with quercetin exhibited a concentration-dependent effect on the inhibition of cell viability.
These findings indicated that quercetin exhibited a protective effect against Aβ-induced cytotoxicity in the PC12 cells. Quercetin provides protection against the cell damaging effects induced by Aβ1 treatment. A3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide assay was used to examine cell viability following quercetin treatment.
Selegiline was used as a positive control. Aβ treatment group. Aβ, amyloid β. By contrast, treatment of the mice with quercetin prior to Aβinjection prevented the behavioral alternations induced by Aβ Quercetin prevents behavior alternations in mice induced by Aβ treatment.
A To examine alternations in behavior, a Y-maze test was used. B To assess the degradation of memory, step-through latency was determined in a passive avoidance task. control group. The learning ability of the mice was examined by measuring response latency, which revealed that treatment of the mice with Aβ led to the degradation of learning ability, compared with the untreated rats.
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