Chlorogenic acid attenuates liver apoptosis and inflammation in endoplasmic reticulum stress-induced mice

Objective(s): The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum results in a state known as “ER stress”. It can affect the fate of proteins and play a crucial role in the pathogenesis of several diseases. In this study, we investigated the protective effect of chlorogenic acid (CA) on the inflammation and apoptosis of tunicamycin-induced ER stress in mice.Materials and Methods: We categorized mice into six groups: Saline, Vehicle, CA, TM, CA ۲۰-TM, and CA ۵۰-TM. The mice received CA (۲۰ or ۵۰ mg/kg) before intraperitoneal tunicamycin injection. After ۷۲ hr of treatment, serum biochemical analysis, histopathological alterations, protein and/or mRNA levels of steatosis, and inflammatory and apoptotic markers were investigated by ELISA and/or RT-PCR. Results: We found that ۲۰ mg/kg CA decreased mRNA levels of Grp۷۸, Ire-۱, and Perk. Moreover, CA supplementation prevented TM-induced liver injury through changes in lipid accumulation and lipogenesis markers of steatosis (Srebp-۱c, Ppar-α, and Fas), and exerted an inhibitory effect on inflammatory (NF-κB, Tnf-α, and Il-۶) and apoptotic markers (caspase ۳, p۵۳, Bax, and Bcl۲), of liver tissue in ER stress mice. Conclusion: These data suggest that CA ameliorates hepatic apoptosis and inflammation by reducing NF-κB and Caspase ۳ as related key factors between inflammation and apoptosis.

Keywords:

Apoptosis , Chlorogenic acid , ER stress , Inflammation , Steatosis