Quercetin improves myocardial redox status in rats with type 2 diabetes

Abstract

Objective. Emerging data indicate that oxidative stress is closely associated with the pathogenesis of cardiovascular disease in type 2 diabetes mellitus (T2DM). The present study aimed to assess the effect of the most abundant flavonoid in the human diet quercetin (Q) on the myocardial redox status in rats with T2DM. Methods. T2DM was induced in male Wistar rats by a high caloric diet (for 14 weeks) and two streptozotocin (25 mg/kg b.w.) injections applied in four weeks of the diet, once a week for two weeks. The Q was administered intragastrically by gavage in a dose of 10 or 50 mg/kg of the body weight for 8 weeks starting from the 8th day after the last streptozotocin injection. The control rats received citrate buffer and seven days after the last STZ injection, basal glucose levels were measured in all animals. Results. Administration of Q increased insulin sensitivity in diabetic rats with more pronounced effect at a dose of 50 mg/kg b.w. The Q also decreased free radical oxidation in the heart mitochondria of diabetic animals, thus limiting the formation of advanced oxidation protein products in a dose-dependent manner and normalized the activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase) in cardiac mitochondria independently of the dose used. In addition, the Q in both doses prevented the development of oxidative stress in the T2DM rats cardiomyocytes by reducing NADPH oxidase and xanthine oxidase activities. Conclusions. The findings demonstrate that Q in both doses 10 mg/kg and 50 mg/kg can protect from the development of oxidative stress in cardiomyocytes in the diabetic rats. The present data indicate that the use of Q may contribute to the amelioration of cardiovascular risk in patients with T2DM.

Study The Mechanism of Huangdi Anxiao Capsules In The Treatment of T2DM of Using UPLC-Q-TOF-MSE Combined With Network Pharmacological

“…Quercetin has anti-in ammatory and antidiabetic effects, animal studies have shown that quercetin can improve islet distortion in T2DM mice, especially mitochondrial atrophy and crest loss in pancreaticβ cells (Shuang et al 2016;). In meanwhile, the quercetin prevented the development of oxidative stress in the T2DM rats cardiomyocytes by reducing NADPH oxidase and xanthine oxidase activities (Nataliia et al 2021). Epiberberine has attracted considerable attention due to its anti-hyperglycemic, anti-hyperlipidemic, and anti-in ammatory functions (Xiao et al 2021), in vitro showed that EPI inhibited the proliferation and induced the G2/M phase arrest of HG-induced GMCs and lower blood sugar to treat diabetic nephropathy.…”

Identification of key pathways and mRNAs in interstitial cystitis/bladder pain syndrome treatment with quercetin through bioinformatics analysis of mRNA-sequence data

“…QCT could stimulate the generation of osteoblast markers and calcified nodules and promote the osteogenic differentiation of bone marrow mesenchymal stem cells [ 16 ]. QCT reduced the free radical oxidation in cardiac mitochondria of type 2 diabetes mellitus rats, improved the oxidative stress of cardiomyocytes in rats and reduced cardiovascular risk in patients with type 2 diabetes mellitus [ 18 ]. In the current study, we found that QCT significantly reduced the increase of pro-inflammatory cytokines in rat plasma and damage to bladder tissue induced by LL-37.…”

A Descriptive Review of the Action Mechanisms of Berberine, Quercetin and Silymarin on Insulin Resistance/Hyperinsulinemia and Cardiovascular Prevention

“…In the same model, the work of Khodarahmi et al [110] demonstrated that the antidiabetic impact of Qtn was associated with increased IRS-1 and decreased NOX1 expression levels, together with down regulation of Rac1-GTP, Rac1, HIF-1alpha and ERK1. Qtn also inhibited NADPH oxidase expression or function in a rat polycystic ovary-related IR model [109], in a Dichlorodiphenyltrichloroethane (DDT) liver toxicity model [126] and in rat cardiomyocytes with T2DM induced with a high-calorie diet and streptozocin [113].…”