Cycloastragenol Improves Brain Damage Induced by Sepsis in Rats

The aim of this study was to explore the effects and mechanisms of cycloastragenol in treatment of brain injury induced by sepsis. The SD (n = 60) rats were divided into NC, Model and Cyc groups and divided into 6 h and 12 h time points. The serum of difference groups were collected and TNF-alpha, IL-1 beta and IL-6 concentration measured by Elisa assay. Pathological state of brain tissues was evaluated by HE staining, apoptosis cell rate by TUNEL assay, TLR2, I kappa B alpha, MyD88 and NE-kappa B (p65) protein expression by IHC assay and NF-kappa B (p65) protein localization by immunofluorescence, and observation of organelle injury by transmission electron microscope. Compared with NC group, the TNF-alpha, IL-1 beta and IL-6 concentrations of Model groups were significantly up-regulated (P < 0.05, respectively); With cycloas-tragenol supplement, the TNF-alpha, IL-1 beta and IL-6 concentrations were significantly suppressed in 6 h and 12 h (P < 0.05, respectively). The apoptosis cell rate of Model groups were significantly increased compared with that of NC groups in 6 h and 12 h (P < 0.05, respectively), However, with Cycloastragenol supplement, the apoptosis cell were depressed in Cyc groups in 6 h and 12 h; the TLR2, I kappa B alpha, MyD88 and NF-kappa B (p65) protein expressions of Model groups were significantly stimulated compared with those of NC groups in 6 h and 12 h (P < 0.05, respectively) and the NE-kappa B (p65) nuclear volume were significantly up-regulated (P < 0.05, respectively) in 6 h and 12 h; meanwhile, after the cycloastragenol treatment, the TLR2, I kappa B alpha, MyD88 and NF-kappa B (p65) protein expressions of Model groups were significantly suppressed compared with those of NC groups in 6 h and 12 h (P < 0.05, respectively) and the NF-kappa B (p65) nuclear volume were significantly down-regulated (P < 0.05, respectively) in 6 h and 12 h. In conclusion, cycloas-tragenol improved brain damage induced by sepsis in rats via regulation of TLR2/I kappa B alpha/MyD88/NF-kappa B (p65) pathway.