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Mechanism of protective effect of carnosol on pig intestinal epithelial cells

文献类型： 外文期刊

作者： Jiang, Zhiguo 1 ; Li, Li 2 ; Hou, Lianjie 1 ; Zhou, Zhuoqiang 3 ; Wang, Chong 1 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Natl Engn Res Ctr Breeding Swine Ind, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Peoples R China

2.Guangzhou Technician Coll, 68 Huangshi East Rd, Guangzhou 510642, Peoples R China

3.South China Agr Univ, Coll Mat & Energy, Guangzhou 510642, Peoples R China

关键词： Carnosol; intestinal oxidative stress; Nrf2; ZYM-SIEC02 cells

期刊名称：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY （ 影响因子：0.252； 五年影响因子：1.188 ）

ISSN： 1936-2625

年卷期： 2020 年 13 卷 3 期

页码：

收录情况： SCI

摘要： This study aims to study the protective effect and mechanism of carnosol on intestinal oxidative stress. Porcine intestinal epithelial cells (ZYM-SIEC02) were pretreated with carnosol. Tert-butyl hydroperoxide (t-BHP) was added to stimulate the cells. The cell colonization and viability were detected by Edu staining, MTT, and cell counting kit-8 (CCK8) assays. The expressions of reactive oxygen species (ROS), nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA) in intracellular and oxidative stress were detected. The expression of related genes and proteins in cells was detected by real-time PCR and western blot. The regulatory mechanisms were identified by co-immunoprecipitation (Co-IP) and chromatin immunoprecipitation (CHIP) assays. The results showed that t-BHP reduced cell proliferation and viability, while cells pretreated with carnosol had resistance to t-BHP, decreased intracellular ROS, MDA and NO levels, and increased SOD content. The mRNA and protein levels of heme oxygenase 1/Nuclear respiratory factor 2 (HO-1/Nrf-2) in ZYM-SIEC02 cells treated with carnosol were significantly increased. Nrf2 was able to bind to cell cycle negative regulatory protein p21 Nrf2 could bind to the promoter regions of cyclin D1 (CCND1) and SOD genes. In conclusion, carnosol has a protective effect on intestinal epithelial cells by upregulating the expression of Nrf2 and inhibiting p21 protein to promote the expression of CCND1 and SOD.

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