Salvianolic Acid B Regulates Intestinal Bacterial/Endotoxin Translocation After Intestinal Ischemia/Reperfusion Injury in Rats Through TLR4/MyD88/MAPK Pathway

ABSTRACT Salvianolic acid B (Sal‐B) is a well‐recognized bioactive ingredient showing certain effects against ischemia/reperfusion (I/R) injury in different organs. This article investigated Sal‐B's effects on regulating intestinal bacterial/endotoxin translocation postintestinal I/R injury via the TLR4/MyD88/MAPK pathway in rats. The rat models of intestinal I/R injury were established by reperfusion following 60 min of superior mesenteric artery occlusion. Rats were treated with Sal‐B after I/R operation. The histopathological changes of the intestine were assessed by H&E staining, and intestinal tissue injury was evaluated based on the Chiu's score system. Pro‐inflammatory factor levels (tumor necrosis factor‐α [TNF‐α], interleukin [IL]‐1β, and IL‐6), superoxide dismutase (SOD) activity, malondialdehyde (MDA) level, and myeloperoxidase (MPO) activity in intestinal tissues were measured through ELISA and kits. The bacterial/endotoxin translocation after intestinal I/R injury was detected by bacterial culture of tissues and Limulus Amebocyte Lysate quantitative kits. The TLR4/MyD88/MAPK pathway‐associated protein levels were measured by western blot analysis. The TLR4‐MyD88 interaction was analyzed via co‐immunoprecipitation. Sal‐B attenuated intestinal I/R injury in rats, evidenced by decreased pathological alterations in intestinal tissues, lowered Chiu's histological score, elevated SOD activity, and diminished MDA level, MPO activity, and pro‐inflammatory cytokine levels. Moreover, Sal‐B reduced intestinal I/R‐triggered intestinal bacterial/endotoxin translocation. Sal‐B could downregulate MyD88 by suppressing TLR4. Inhibition of the TLR4/MyD88 pathway alleviated intestinal bacterial/endotoxin translocation, while activation of this pathway partially counteracted the improvement effects of Sal‐B in rats with intestinal I/R injury. Sal‐B impeded the MAPK pathway by repressing TLR4/MyD88. Sal‐B mitigates intestinal I/R‐induced intestinal bacterial/endotoxin translocation in rats by blocking the TLR4/MyD88/MAPK pathway.