Biliary tract external drainage alleviates kidney injury in shock

Abstract

BackgroundKidney injury is common in hemorrhagic shock (HS). Kidney injury leads to a systemic increase in serum chemokines and cytokines and causes injuries to other vital organs. Our previous studies showed that vitamin C led to organ protection and inflammation inhibitory effects in rat models of HS via induction heme oxygenase-1 (HO-1). We also found that biliary tract external drainage (BTED) increased the expression levels of HO-1 in rat livers. We investigated roles of BTED in kidney injury and its relationship with the HO-1 pathway in HS in this research. MethodsRat models of HS were induced by drawing blood from the femoral artery. BTED was performed by inserting a catheter into the bile duct. Thirty-six Sprague–Dawley rats were randomized to sham group; HS group; zinc protoporphyrin IX (Znpp) group; BTED group; BTED + Znpp group, and BTED + bile infusion group. The expression levels of HO-1 in the kidney were analyzed by Western blotting. The expression levels of occludin messenger RNA in the kidney were analyzed by real-time reverse transcription-polymerase chain reaction. The expression levels of occludin in the kidney were analyzed by immunohistochemistry. Histology of renal was performed by hematoxylin and eosin staining. ResultsOccludin messenger RNA and protein levels in the kidney increased markedly after BTED under HS conditions. Renal histopathologic scores decreased significantly after BTED under HS conditions. Znpp significantly inhibited all mentioned effects. ConclusionsBTED alleviates kidney injury in rats of HS via the HO-1 pathway.