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

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.