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白藜芦醇对 HO 暴露的永生化鸭小肠上皮细胞的保护作用。

Protective Effect of Resveratrol on Immortalized Duck Intestinal Epithelial Cells Exposed to HO.

机构信息

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Institute of Animal Science & Veterinary, Zhejiang Academy of Agricultural Sciences, Hangzhou 310000, China.

College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Molecules. 2022 May 31;27(11):3542. doi: 10.3390/molecules27113542.

DOI:10.3390/molecules27113542
PMID:35684483
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9182484/
Abstract

Resveratrol is a polyphenolic compound with anti-oxidation effects. The mechanisms underlying the antioxidant effects of resveratrol in duck intestinal epithelial cells remain unclear. The protective effects of resveratrol against oxidative stress induced by H2O2 on immortalized duck intestinal epithelial cells (IDECs) were investigated. IDECs were established by transferring the lentivirus-mediated simian virus 40 large T (SV40T) gene into small intestinal epithelial cells derived from duck embryos. IDECs were morphologically indistinguishable from the primary intestinal epithelial cells. The marker protein cytokeratin 18 (CK18) was also detected in the cultured cells. We found that resveratrol significantly increased the cell viability and activity of catalase and decreased the level of intracellular reactive oxygen species and malondialdehyde, as well as the apoptosis rate induced by H2O2 (p < 0.05). Resveratrol up-regulated the expression of NRF2, p-NRF2, p-AKT, and p-P38 proteins and decreased the levels of cleaved caspase-3 and cleaved caspase-9 and the ratio of Bax to Bcl-2 in H2O2-induced IDECs (p < 0.05). Our findings revealed that resveratrol might alleviate oxidative stress by the PI3K/AKT and P38 MAPK signal pathways and inhibit apoptosis by altering the levels of cleaved caspase-3, cleaved caspase-9, Bax, and Bcl-2 in IDECs exposed to H2O2.

摘要

白藜芦醇是一种具有抗氧化作用的多酚化合物。白藜芦醇在鸭肠上皮细胞中抗氧化作用的机制尚不清楚。本研究旨在探讨白藜芦醇对 H2O2 诱导的鸭肠上皮细胞(IDECs)氧化应激的保护作用。通过将慢病毒介导的猿猴病毒 40 大 T (SV40T)基因转染入鸭胚胎小肠上皮细胞,建立 IDECs 细胞系。转染后的 IDECs 细胞在形态上与原代肠上皮细胞无明显差异,且培养的细胞中也检测到了细胞角蛋白 18 (CK18)标志物蛋白。结果发现,白藜芦醇可显著提高细胞活力和过氧化氢酶活性,降低细胞内活性氧和丙二醛水平,降低 H2O2 诱导的细胞凋亡率(p < 0.05)。白藜芦醇还可上调 NRF2、p-NRF2、p-AKT 和 p-P38 蛋白的表达,降低 H2O2 诱导的 IDECs 中 cleaved caspase-3 和 cleaved caspase-9 的水平,以及 Bax/Bcl-2 的比值(p < 0.05)。综上所述,白藜芦醇可能通过 PI3K/AKT 和 P38 MAPK 信号通路减轻氧化应激,并通过改变 cleaved caspase-3、cleaved caspase-9、Bax 和 Bcl-2 的水平抑制 IDECs 凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396c/9182484/502b8b554258/molecules-27-03542-g008.jpg
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