All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Apoptosis in IPEC-J2 Cells via Inhibiting ROS-Mediated P38MAPK Signaling Pathway

被引：15

作者：

Pu, Junning ^{[1
]}

Chen, Daiwen ^{[1
]}

Tian, Gang ^{[1
]}

He, Jun ^{[1
]}

Huang, Zhiqing ^{[1
]}

Zheng, Ping ^{[1
]}

Mao, Xiangbing ^{[1
]}

Yu, Jie ^{[1
]}

Luo, Junqiu ^{[1
]}

Luo, Yuheng ^{[1
]}

Yan, Hui ^{[1
]}

Yu, Bing ^{[1
]}

机构：

[1] Sichuan Agr Univ, Minist Educ, Inst Anim Nutr, Key Lab Anim Disease Resistance Nutr, Chengdu 611130, Peoples R China

来源：

ANTIOXIDANTS | 2022年 / 11卷 / 02期

关键词：

all-trans retinoic acid; transmissible gastroenteritis virus; apoptosis; oxidative stress; ROS; P(38)MAPK pathway; IPEC-J2; cells; OXIDATIVE STRESS; ACTIVATION; EXPRESSION; MITOCHONDRIAL; OXYGEN; DEATH; FAS;

D O I：

10.3390/antiox11020345

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Transmissible gastroenteritis virus (TGEV) can cause diarrhea, dehydration, and high mortality in piglets, which is closely related to intestinal epithelial cell apoptosis caused by TGEV infection. All-trans retinoic acid (ATRA) is the active metabolite of vitamin A, which has antioxidant and anti-apoptotic properties. However, it is unknown whether ATRA can attenuate TGEV-induced IPEC-J2 cells apoptosis. Therefore, we investigated the protective effects of ATRA on TGEV-induced apoptosis of IPEC-J2 cells and explored the potential molecular mechanism. Our results indicated that TGEV infection caused IPEC-J2 cells damage and apoptosis. However, ATRA treatment attenuated TGEV-induced IPEC-J2 cells damage by upregulating the mRNA expressions of ZO-1, Occludin, and Mucin-1. ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P(38)MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). In addition, treatment of TGEV-infected IPEC-J2 cells with the ROS inhibitors (NAC) significantly reduced the protein levels of p-P(38)MAPK, Fas, Bax, and Cleaved-caspase-3 and the percentage of apoptotic cells. Our results indicated that ATRA attenuated TGEV-induced apoptosis in IPEC-J2 cells via improving the antioxidant capacity, thereby inhibiting the cell damage. the mechanism of which is associated with the inhibition of ROS-mediated P(38)MAPK signaling pathway.

引用

页数：16