Salidroside mitigates experimental colitis through cyclic adenosine monophosphate pathway activation and suppression of enteric glial cell responses

Figure 7 Salidroside inhibited enteric glial cells activation in the myenteric plexus and submucosal plexus through cyclic adenosine monophosphate/protein kinase A/cyclic adenosine monophosphate-response element binding protein signaling and reduced intestinal inflammation in dextran sulfate sodium salt-induced colitis. A-H: Immunofluorescent histochemistry double-staining of mouse colonic myenteric plexus (MP) (A-D) and submucosal plexus (SP) (E-H). The magnified images show the corresponding white square areas in greater detail. The white arrows indicate glial fibrillary acidic protein-positive enteric glial cells (EGCs). Control group (A and E); Dextran sulfate sodium salt (DSS) group (B and F); DSS + salidroside (Sal) group (C and G); DSS + Sal + H89 group (D and H); I: The number of Hu C/D positive enteric neurons in the MP was subjected to quantitative analysis; J: The area exhibiting apparent overlap of EGCs processes with the neurons in the MP; K: The number of Hu C/D positive enteric neurons in the SP was subjected to quantitative analysis; L: The area exhibiting apparent overlap of EGCs processes with the neurons in the SP; M-P: Comparison of interleukin (IL)-1β (M), IL-6 (N), necrosis factor-α (O) and nuclear factor kappa-B (P) expression levels in peripheral blood of the four groups of mice. Data are shown as mean ± SEM (n = 4), P values were calculated using one-way analysis of variance with Tukey’s test for Figure 7I-P. ^aP < 0.05. ^bP < 0.01. DSS: Dextran sulfate sodium salt; Sal: Salidroside; EGC: Enteric glial cell; IL: Interleukin; TNF: Tumor necrosis factor; NF-κB: Nuclear factor kappa-B; DAPI: 4’,6-diamidino-2-phenylindole; GFAP: Glial fibrillary acidic protein.