Fig. 2

Post-stroke intestinal changes and their impacts on cerebral organization. Stroke causes a reduction in the expression of intestinal epithelial tight junction proteins including VE-cadherin, Occludin and Claudin-5; more LPS is produced by post-stroke intestinal flora, which induces damage by binding to TLR4/MyD88 in the downstream inflammatory response; LPS also contributes to an increase in eNOS-P/total eNOS, causing vascular endothelial damage; stroke causes an increase in miR-21-5p and further upregulated ARF4; the aforementioned factors combined lead to increased intestinal mucosal permeability and leaky gut. The blood LPS, DAO and D-LAC elevated after vascular endothelial injury and BBB endothelial injury accompanied by VIPR1/2 decreasing