RESUMEN
Objectives: The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER)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 20-TM, and CA 50-TM. The mice received CA (20 or 50 mg/kg) before intraperitoneal tunicamycin injection. After 72 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 20 mg/kg CA decreased mRNA levels of Grp78, Ire-1, and Perk. Moreover, CA supplementation prevented TM-induced liver injury through changes in lipid accumulation and lipogenesis markers of steatosis (Srebp-1c, Ppar- α , and Fas), and exerted an inhibitory effect on inflammatory (NF- κ B, Tnf- α , and Il-6) and apoptotic markers (caspase 3, p53, Bax, and Bcl2), of liver tissue in ER stress mice. Conclusion: These data suggest that CA ameliorates hepatic apoptosis and inflammation by reducing NF-κB and Caspase 3 as related key factors between inflammation and apoptosis.
