The double-stranded RNA-dependent protein kinase (PKR) is involved in inflammatory cytokine expression and disease pathogenesis in many conditions. The aim of this study was to explore the role of PKR in sepsis-induced renal tissue injury. Six-week-old C57BL/6J mice received PKR inhibitor (imoxin) and Endoplasmic reticulum (ER) inducer (tunicamycin) 2 hr prior to induction of inflammation via cecal ligation and puncture (CLP). Renal tissues were collected 24 hr after the CLP treatment and protein expression were assessed. The expression of creatinine (Cre) and blood urea nitrogen (BUN) in serum and inflammation factor in tissues was detected by ELISA, and the apoptosis of renal tissue was detected by TUNEL staining. PKR inhibitors reduce the expression of sepsis-induced ER stress in renal tissue, as well as the pathological changes and renal impairment in renal tissue. PKR inhibitors reduce the expression of sepsis-induced inflammatory response and sepsis-induced apoptosis in renal tissue by ER stress. In conclusion, PKR inhibitor alleviates ER stress and alleviates sepsis-induced renal injury.
Keywords: Endoplasmic reticulum stress; Renal injury; Sepsis; Double-stranded RNA-dependent protein kinase.