The Protection Of Shenmai Combined Ligustrazine Injection On Liver In Sepsis Mice

Objective To investigate the protective effect and mechanisms of Shenmai combined Ligustrazine injection on sepsis-induced liver injury in mice.Method Sepsis-induced liver injury was induced by cecal ligation and puncture(CLP) in KunMing mice.Male mice were randomly divided into sham operation group(group A),model group(group B),Shenmai injection group(group C),Ligustrazine injection group(group D) and Shenmai combined Ligustrazine injection group(group E). Animals received a separate intraperitoneal injection of Shenmai and Ligustrazine injection or normal saline at24h,12h and1h before CLP.The changes and injury of liver tissue was evaluated by HE staining.Survival curves were obtained by the Kaplan-Meier method.The activity of ALT/AST,MPO,iNOS and the content of MDA,NO was detected by biochemistry enzymology.The changes of IL-6and TNF-α expression in mice serum was detected by ELISA.NOD1,NOD2mRNA expressions in liver were detected by RT-PCR and NF-κb protein expressions in liver were detected by Western-blotting.Results The survival rate of mice were significantly higher and pathological injury of liver was distinctively alleviativer in the group C,D and E than that in group B. And in these three treatment groups,the levels of ALT,AST,IL-6,TNF-α in serum and MPO,MDA,NO,,iNOS in liver tissue were lowered obviously,as compared with group B.It was worth of pointing out that Shenmai combined Ligustrazine injection showed the best therapeutic action to sepsis mice. Furthermore,in group E the levels of serum pro-inflammatory cytokine(TNF-α,IL-6)were remarkably decreased as compared with group C and D. Shenmai, Ligustrazine injection and Shenmai combined Ligustrazine injection obviously inhibited the over expression of NF-κb protein and NOD1and NOD2mRNA, especially Shenmai combined Ligustrazine injection.Conclusion It is suggested that Shenmai combined Ligustrazine injection has a protective effect on sepsis-induced liver injury in mice. Inhibiting the over expression of NOD and NOD2, preventing NF-κb activating and decreasing systemic inflammation may be involved in the protective mechanism.