Open AccessCelecoxib attenuates hepatocyte apoptosis by inhibiting endoplasmic reticulum stress in thioacetamide-induced cirrhotic rats
Author(s) -
Su Wei,
Yang Tai,
Shihang Tang,
Yanting Ye,
Chong Zhao,
Jinhang Gao,
Biguang Tuo,
Chengwei Tang
Publication year - 2020
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v26.i28.4094
Subject(s) - endoplasmic reticulum , thioacetamide , apoptosis , hepatocyte , celecoxib , medicine , unfolded protein response , chemistry , pharmacology , cancer research , endocrinology , microbiology and biotechnology , biology , biochemistry , in vitro
Endoplasmic reticulum (ER) stress is an important mechanism in the progression of chronic and acute liver diseases, especially in the progression and recovery of liver fibrosis. Excessive and long-term ER stress induces apoptosis. ER stress-induced apoptosis is considered to be an important pathway in the development of liver fibrosis. Cyclooxygenase-2 (COX-2) induction is also closely related to ER stress. In our previous studies, we showed that celecoxib, a COX-2 inhibitor, improves liver fibrosis and portal hypertension. However, the role and mechanism of celecoxib in alleviating liver fibrosis remain unclear.