title: Quercetin and quercitrin protect against cytokine‑induced injuries in             RINm5F β-cells via the mitochondrial pathway and NF-κB signaling.
abstract: Quercetin, existing mostly in its glycoside form quercitrin, is the most             widely distributed flavonoid in nature. It possesses various potential effects             as an antioxidant, anti-inflammatory for cell damage of β-cells, however, studies             on this topic are limited and controversial. In order to examine the effects of             quercetin on type I diabetes mellitus, we investigated the role of quercetin/quercitrin             in cytokine-induced β-cell injuries in RINm5F rat insulinoma cells. Cell viability,             glucose-stimulated insulin secretion (GSIS), intracellular reactive oxygen species             (ROS), nitric oxide (NO) and inflammation or apoptosis-associated protein expression             were measured with or without quercetin/quercitrin treatment. We also compared             the differences between the aglycone and the glycoside forms of quercetin, with             the aim to shed some light on their structures and transportation into cells.             The results showed that quercetin/quercitrin protected against cytokine-induced             cell death, improved GSIS, and inhibited ROS as well as NO accumulation. These             effects were associated with reduced expression of inducible nitric oxide synthases             (iNOS) and inhibited translocation of nuclear factor-κB (NF-κB). Also, quercetin/quercitrin             suppressed cytochrome c release from mitochondria and the following alteration             of downstream proteins, suggesting that mitochondrial apoptosis was attenuated             by quercetin treatment. In summary, quercetin and quercitrin are potential candidates             to prevent β-cell death via the mitochondrial pathway and NF-κB signaling, and             quercetin may be more efficacious than quercitrin as an anti-diabetic agent.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University Health Science Center, Haidian, Beijing 100191, PR China.
authors.forename: Xiaoqian
authors.initials: X
authors.lastname: Dai
authors.forename: Ye
authors.initials: Y
authors.lastname: Ding
authors.forename: Zhaofeng
authors.initials: Z
authors.lastname: Zhang
authors.forename: Xiaxia
authors.initials: X
authors.lastname: Cai
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D045304:Cytochromes c / Q000378:metabolism; D016207:Cytokines / Q000009:adverse effects*; D005947:Glucose / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007340:Insulinoma / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017382:Reactive Oxygen Species; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D007004:Hypoglycemic Agents; D007328:Insulin; D016328:NF-kappa B; D017382:Reactive Oxygen Species; C012526:quercitrin; D009569:Nitric Oxide; D045304:Cytochromes c; D011794:Quercetin; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D005947:Glucose