Diabetes exacerbated sepsis-induced intestinal injury by promoting M1 Macrophage Polarization via miR-3061/Snail1 signaling.

Sepsis is a severe clinical syndrome related to an exaggerated host immune response to infection as well as systematic inflammation and serious tissue damage. Sepsis-induced intestine injury is one of the most frequent and serious complications of sepsis. This study aimed to identify new mechanisms in sepsis-induced intestine injury through transcriptome profiling (RNA-seq). A total of 5 C57BL/6 mice were randomly divided into 2 groups: CLP group (n=3), Sham group (n=2).The disinfected abdomen was incised 1 cm at midline to expose the cecum. Silk thread was subsequently used to ligate the proximal third of the cecum. Then punctured with a 22G needle once a time and extruded fecal matter. Finally, the cecum was inserted back into abdomen and the incision was sutured. After surgery, 4ml/100g normal saline was injected subcutaneously for fluid resuscitation. In addition, bupivacaine and Butorphanol Tartrate was used for postoperatively analgesia. The cecum was only exposed and then returned to the abdomen in the two sham groups. The serum and intestinal tissue were collected at 12h after surgery. Examination of 2 different groups in RAW264.7 cells. GL group (n=2), Sham group (n=2). RAW264.7 cells in GL group were stimulated with high glucose and LPS.