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甜菜红素通过 Nrf2 信号通路减轻 STZ 诱导的糖尿病大鼠肝脏的氧化应激。

Betanin alleviates oxidative stress through the Nrf2 signaling pathway in the liver of STZ-induced diabetic rats.

机构信息

Department of Clinical Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

Student Research Committee, Zanjan University of Medical Sciences, Zanjan, Iran.

出版信息

Mol Biol Rep. 2022 Oct;49(10):9345-9354. doi: 10.1007/s11033-022-07781-8. Epub 2022 Aug 21.

DOI:10.1007/s11033-022-07781-8
PMID:35988103
Abstract

BACKGROUND

Continuing hyperglycemia causes and exacerbate oxidative stress. Betanin as the principal pigment of red beet root has antioxidant, anti-inflammatory, and anti-diabetic properties. The purpose of this study was to investigate the potency of betanin on antioxidant defense in STZ-induced diabetic rats' livers.

METHODS

STZ at a single dose of 60 mg/kg body weight was intraperitoneally injected and betanin (10, 20, and 40 mg/kg/day) was administered orally for 28 days. Malondialdehyde (MDA), total antioxidant capacity (TAC), protein carbonyl (PC) levels, and the enzyme activity of superoxide dismutase (SOD), catalases and glutathione peroxidases (GPx) were evaluated in the liver. Furthermore, gene expression of Nrf2 and mentioned antioxidant enzymes were measured by Real-time PCR.

RESULTS

Betanin (10 and 20 mg/kg) significantly reduced PC levels and increased antioxidant enzyme activity in diabetic rats compared to the control diabetic group (P < 0.01). In comparison to the diabetic control group, all studied genes expression in diabetic rats were increased significantly with betanin at doses of 10 and 20 mg/kg (P < 0.02). The increase in gene expression at 20 mg/kg of betanin was significantly stronger than others (P < 0.015) except for the catalase (P = 0.201), that was almost the same. Moreover, treatment of diabetic rats with 20 mg/kg of betanin could significantly increase TAC levels (P < 0.05) and decrease MDA levels (P < 0.001) compared to diabetic control group.

CONCLUSIONS

Betanin could increase the antioxidant capacity of liver tissue associated with the Nrf2-mediated pathway in a dose-dependent manner.

摘要

背景

持续的高血糖会导致并加剧氧化应激。甜菜红的主要色素甜菜苷具有抗氧化、抗炎和抗糖尿病的特性。本研究旨在探讨甜菜苷对 STZ 诱导的糖尿病大鼠肝脏抗氧化防御系统的作用。

方法

一次性腹腔注射 STZ60mg/kg 体重,连续 28 天给予甜菜苷(10、20 和 40mg/kg/天)灌胃。检测肝脏中丙二醛(MDA)、总抗氧化能力(TAC)、蛋白羰基(PC)水平以及超氧化物歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶(GPx)的酶活性。此外,通过实时 PCR 测量 Nrf2 和抗氧化酶的基因表达。

结果

与对照组糖尿病大鼠相比,甜菜苷(10 和 20mg/kg)可显著降低糖尿病大鼠的 PC 水平并增加抗氧化酶活性(P<0.01)。与糖尿病对照组相比,糖尿病大鼠的所有研究基因表达均随着甜菜苷剂量的增加(10 和 20mg/kg)而显著增加(P<0.02)。与其他剂量相比,甜菜苷(20mg/kg)对基因表达的增加更为明显(P<0.015),除了过氧化氢酶(P=0.201)几乎相同。此外,与糖尿病对照组相比,20mg/kg 甜菜苷治疗可显著增加 TAC 水平(P<0.05)并降低 MDA 水平(P<0.001)。

结论

甜菜苷可通过 Nrf2 介导的途径以剂量依赖的方式增加肝脏组织的抗氧化能力。

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