Quercitrin

Quercitrin ameliorates cytokine-impaired viability of RINm5F cells and improves Glucose-stimulated insulin secretion in cytokine-treated RINm5F cells. It also reduces production of cellular ROS from cytokines and restrains the enhancement of NO production caused by cytokines in RINm5F cells via inhibition of iNOS expression^[1].

Cells are cultured in DMEM with 10% FBS, 100 U/ml penicillin, 100 μg/ml streptomycin, 2 mmol/l in a humidified atmosphere (5% CO2, 37°C). After starvation for 24 h, cells are treated with quercetin or quercitrin (0, 5, 10 and 20 μM) for 2 h, then co-incubated with TNF-α (10 ng/ml), IL-1β (5 ng/ml) and IFN-γ (1,000 U/ml) for 24 h.

Quercitrin significantly suppresses the elevation of reactive oxygen species (ROS) production and malondialdehyde (MDA) content, reduces tissue plasminogen activator (t-PA) activity, enhances the antioxidant enzyme activities and abrogates cytochrome P450 2E1 (CYP2E1) induction in mouse brains. Quercitrin also prevents CCl4 induced cerebral function disorders associated with its ability to inhibit the activities of monoamine oxidase (MAO), acetylcholine esterase (AChE) and the N-methyl-D-aspartate receptor 2B subunit (NR2B). Quercitrin is known to have biological effects such as anti-oxidative, anti-inflammatory, and anti-apoptosis effects and it might be a more potent antioxidant and a neuroprotective agent than quercetin due to its high bioavailability in the digestive track. Quercitrin significantly reduces acute systemic inflammation in LPS-induced models as well as attenuates inflammation in the livers of mice. Quercitrin could also reduce inflammation and apoptosis in cytokine-induced models. In streptozotocin (STZ)-induced diabetic models, quercitrin displays organ protective properties in the pancreas, liver and kidney by improving the antioxidant status^[2].