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白藜芦醇对高糖诱导的HepG2细胞氧化应激和凋亡的保护作用。

The protective role of resveratrol against high glucose-induced oxidative stress and apoptosis in HepG2 cells.

作者信息

Tshivhase Abegail Mukhethwa, Matsha Tandi, Raghubeer Shanel

机构信息

SAMRC/CPUT Cardiometabolic Health Research Unit, Department of Biomedical Sciences, Faculty of Health and Wellness Sciences Cape Peninsula University of Technology Bellville South Africa.

Sefako Makgatho Health Sciences University Ga-Rankuwa South Africa.

出版信息

Food Sci Nutr. 2024 Feb 16;12(5):3574-3584. doi: 10.1002/fsn3.4027. eCollection 2024 May.

DOI:10.1002/fsn3.4027
PMID:38726423
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11077230/
Abstract

High glucose concentrations result in oxidative stress, leading to damage of cellular constituents like DNA, proteins, and lipids, ultimately resulting in apoptosis. Resveratrol, a polyphenol phytoalexin, has been studied for its potential therapeutic effects on diabetes. This study investigated the influence of high glucose (HG) on HepG2 cells and assessed resveratrol's effect on high-glucose-induced oxidative stress and apoptosis. HepG2 cells were cultured for 48 and 72 h with high glucose (40 mM), low resveratrol (25 μM), high resveratrol (50 μM), high glucose + low resveratrol, and high glucose + high resveratrol. After exposure, oxidative and apoptosis-related gene expression was evaluated using quantitative polymerase chain reaction (qPCR), and lactate dehydrogenase (LDH) release was measured using the supernatant. In HepG2 cells cultured with high glucose, all antioxidant enzymes (SOD, superoxide dismutase; GPx1, glutathione peroxidase 1; CAT, catalase; Nrf2, nuclear factor erythroid 2-related factor 2; and NQO1, NAD(P)H quinone oxidoreductase 1) were significantly reduced; however, when HepG2 cells were cultured with resveratrol (25 and 50 μM) and high glucose, the expression levels of all antioxidant enzymes were increased. The anti-apoptotic gene (B-cell lymphoma 2; ) and the DNA repair gene (Oxoguanine glycosylase-1, ) were significantly decreased following high glucose exposure to HepG2 cells. Surprisingly, the expression levels of and were notably elevated after resveratrol treatment. Furthermore, high glucose levels increased the LHD release in HepG2 cells, whereas resveratrol treatment reduced the LDH release. Our results demonstrate that resveratrol provides protection against oxidative stress and apoptosis induced by high glucose in HepG2 cells. Hence, resveratrol shows potential as an effective approach to address the impaired antioxidant response resulting from elevated glucose levels commonly observed in diabetes and metabolic disorders.

摘要

高葡萄糖浓度会导致氧化应激,进而损害细胞成分,如DNA、蛋白质和脂质,最终导致细胞凋亡。白藜芦醇是一种多酚类植物抗毒素,其对糖尿病的潜在治疗作用已得到研究。本研究调查了高糖(HG)对HepG2细胞的影响,并评估了白藜芦醇对高糖诱导的氧化应激和细胞凋亡的作用。将HepG2细胞分别用高糖(40 mM)、低剂量白藜芦醇(25 μM)、高剂量白藜芦醇(50 μM)、高糖+低剂量白藜芦醇以及高糖+高剂量白藜芦醇培养48小时和72小时。处理后,使用定量聚合酶链反应(qPCR)评估氧化和凋亡相关基因的表达,并使用上清液测量乳酸脱氢酶(LDH)释放。在用高糖培养的HepG2细胞中,所有抗氧化酶(超氧化物歧化酶SOD、谷胱甘肽过氧化物酶1 GPx1、过氧化氢酶CAT、核因子红细胞2相关因子2 Nrf2以及NAD(P)H醌氧化还原酶1 NQO1)均显著降低;然而,当HepG2细胞与白藜芦醇(25和50 μM)及高糖一起培养时,所有抗氧化酶的表达水平均升高。高糖处理HepG2细胞后,抗凋亡基因(B细胞淋巴瘤2)和DNA修复基因(氧化鸟嘌呤糖基化酶-1)显著降低。令人惊讶的是,白藜芦醇处理后,这两个基因的表达水平显著升高。此外,高糖水平增加了HepG2细胞中LHD的释放,而白藜芦醇处理则降低了LDH的释放。我们的结果表明,白藜芦醇可保护HepG2细胞免受高糖诱导的氧化应激和细胞凋亡。因此,白藜芦醇显示出作为一种有效方法来解决糖尿病和代谢紊乱中常见的因血糖升高导致的抗氧化反应受损的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/5b06f662f490/FSN3-12-3574-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/1afd6f3e194a/FSN3-12-3574-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/7d4d06ffcd13/FSN3-12-3574-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/dcf76d64dcdc/FSN3-12-3574-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/5b06f662f490/FSN3-12-3574-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/1afd6f3e194a/FSN3-12-3574-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/7d4d06ffcd13/FSN3-12-3574-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/dcf76d64dcdc/FSN3-12-3574-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/11077230/5b06f662f490/FSN3-12-3574-g001.jpg

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