Abstract
BackgroundRotavirus (RV) is a major pathogen that causes severe gastroenteritis in infants and young animals. Endoplasmic reticulum (ER) stress and subsequent apoptosis play pivotal role in virus infection. However, the protective mechanisms of intestinal damage caused by RV are poorly defined, especially the molecular pathways related to enterocytes apoptosis. Thus, the aim of this study was to investigate the protective effect and mechanism of sodium butyrate (SB) on RV-induced apoptosis of IPEC-J2 cells.ResultsThe RV infection led to significant cell apoptosis, increased the expression levels of ER stress (ERS) markers, phosphorylated protein kinase-like ER kinase (PERK), eukaryotic initiation factor 2 alpha (eIF2α), caspase9, and caspase3. Blocking PERK pathway using specific inhibitor GSK subsequently reversed RV-induced cell apoptosis. The SB treatment significantly inhibited RV-induced ERS by decreasing the expression of glucose regulated protein 78 (GRP78), PERK, and eIF2α. In addition, SB treatment restrained the ERS-mediated apoptotic pathway, as indicated by downregulation of C/EBP homologous protein (CHOP) mRNA level, as well as decreased cleaved caspase9 and caspase3 protein levels. Furthermore, siRNA-induced GPR109a knockdown significantly suppressed the protective effect of SB on RV-induced cell apoptosis.ConclusionsThese results indicate that SB exerts protective effects against RV-induced cell apoptosis through inhibiting ERS mediated apoptosis by regulating PERK-eIF2α signaling pathway via GPR109a, which provide new ideas for the prevention and control of RV.
Highlights
Rotavirus (RV) is the main cause of viral gastroenteritis in infants, young children, and young animals around the globe [1,2,3], which RV infection results in 12,000 to 15,000 annual deaths among children under 5 years each year [4, 5]
RV induces ER stress (ERS) mediated apoptosis in IPEC-J2 cells Initially, to define whether RV induce ERS mediated cell apoptosis, different assays were conducted in uninfectedand RV-infected IPEC-J2 cells at 24 h post-infection
sodium butyrate (SB) ameliorates RV induced ERS mediated apoptosis in IPEC-J2 cells To determine whether SB could exert a protective effect against RV induced cell apoptosis
Summary
Rotavirus (RV) is the main cause of viral gastroenteritis in infants, young children, and young animals around the globe [1,2,3], which RV infection results in 12,000 to 15,000 annual deaths among children under 5 years each year [4, 5]. The detrimental effects of RV on public health have prompted substantial concern about how to efficiently protect the human or animal against RV infection. Rotavirus (RV) is a major pathogen that causes severe gastroenteritis in infants and young animals. The protective mechanisms of intestinal damage caused by RV are poorly defined, especially the molecular pathways related to enterocytes apoptosis. The aim of this study was to investigate the protective effect and mechanism of sodium butyrate (SB) on RV-induced apoptosis of IPEC-J2 cells
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