4.6 Article

Protective Effect of Resveratrol on Immortalized Duck Intestinal Epithelial Cells Exposed to H2O2

期刊

MOLECULES
卷 27, 期 11, 页码 -

出版社

MDPI
DOI: 10.3390/molecules27113542

关键词

resveratrol; epithelial cells; duck; oxidative stress; apoptosis

资金

  1. National Natural Science Foundation of China [32172688]
  2. China Agriculture Research System of MOF and MARA [CARS-42-6]
  3. Zhejiang Science and Technology Major Program on Agricultural New Variety Breeding [2021C02068-10]

向作者/读者索取更多资源

Resveratrol has antioxidant effects on duck intestinal epithelial cells, potentially alleviating oxidative stress and inhibiting cell apoptosis through the PI3K/AKT and P38 MAPK signaling pathways. These findings have important implications for studying the health benefits of resveratrol.
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.

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