Protective effects of sodium butyrate on rotavirus inducing endoplasmic reticulum stress-mediated apoptosis via PERK-eIF2α signaling pathway in IPEC-J2 cells

Abstract Background Rotavirus (RV) is a major pathogen that causes severe gastroenteritis in infants and young animals. Endoplasmic reticulum (ER) stress subsequent apoptosis play pivotal role virus infection. However, the protective mechanisms of intestinal damage caused by RV are poorly defined, especially molecular pathways related to enterocytes apoptosis. Thus, aim this study was investigate effect mechanism sodium butyrate (SB) on RV-induced IPEC-J2 cells. Results The infection led significant cell apoptosis, increased expression levels ER (ERS) markers, phosphorylated protein kinase-like kinase ( PERK ), eukaryotic initiation factor 2 alpha eIF2α caspase9, caspase3. Blocking pathway using specific inhibitor GSK subsequently reversed SB treatment significantly inhibited ERS decreasing glucose regulated 78 GRP78 , . In addition, restrained ERS-mediated apoptotic pathway, as indicated downregulation C/EBP homologous CHOP ) mRNA level, well decreased cleaved caspase9 caspase3 levels. Furthermore, siRNA-induced GPR109a knockdown suppressed Conclusions These results indicate exerts effects against through inhibiting mediated regulating PERK-eIF2α signaling via GPR109a, which provide new ideas for prevention control RV.