| Sepsis-associated encephalopathy(SAE)is a diffuse cerebral dysfunction which resulted in sepsis generated by non-central system infection.When patients with sepsis are complicated with cerebral dysfunction,the mortality will increase significantly.Meanwhile,septic encephalopathy can not only cause short-term reversible central nervous system dysfunction,but also cause long-term irreversible cognitive disorder.Early and appropriate treatment for patients with confirmed sepsis encephalopathy will significantly reduce the mortality of patients and improve their long-term prognosis.However,there are still no effective drugs in clinical treatment of sepsis encephalopathy,so it is extremely urgent to explore new effective treatment methods.As a natural inhibitor of high mobility group box-1(hmgb-1),the anti-inflammatory effect of glycyrrhizin has attracted more and more attention in recent years.Glycyrrhizic acid has been shown to play a therapeutic role in inflammatory diseases such as infection,pancreatitis and ulcerative colitis.At the same time,studies have also shown that glycyrrhizic acid can penetrate through the blood-brain barrier of normal rats,and further studies have found that when brain tissue is damaged,the surrounding blood-brain barrier will be weakened or destroyed,making glycyrrhizic acid more likely to penetrate into the injured brain tissue and inhibiting the expression and secretion of hmgb-1 protein in rats with brain injury.Diammonium glycyrrhizinate is a new generation of liquorice extract,which has better stability,higher solubility and stronger biological activity than traditional glycyrrhizic acid preparations.But there is still a lack of research on the therapeutic effect of diammonium glycyrrhizinate on SAE rats at present.Therefore,this study aims to explore the therapeutic effect of diammonium glycyrrhizinate on SAE rats and explore the possible mechanism.Objective: To explore the therapeutic effect of diammonium glycyrrhizinate on SAE rats and the possible mechanism,in order to provides a certain theoretical basis for clinical exploration of SAE treatment methods.Methods:(1)grouping and modeling: SD rats were divided into sham operation group(S group),SAE group(group C)and SAE+ Diammonium glycyrrhizinate group(group D).Model establishment: SAE model was established by cecal ligation perforation(CLP)after adaptive feeding.At 30 min and 24 h after establish SAE model,rats in group D were given diammonium glycyrrhizinate by gavage at 120mg/kg.(2)MORRIS water maze experiment was used to evaluate the activity,learning and memory of rats.(3)Western blot analysis were performed to detect the expression of HMGB-1,IL-1b,IL-6,and TNF-α protein.Results: MORRIS water maze experiment: In the place navigation test,the escape latency of rats in group S and group D were shorter compared with that in group C,and the difference was statistically significant(P < 0.05),while the swimming speed of rats between the three groups was not significantly different.Moreover,as the number of days increased,the escape latency of rats in each group were shortened,which most has statistically significance(P < 0.05).In the spatial probe test,the number of passes in group S and group D crossing the original platform was increased compared with that in group C,and the activity time in the target quadrant was prolonged,all the differences have significance in statistics(P < 0.05).The results of Western blot showed that the levels of hmgb-1,il-1b,il-6 and TNFproteins in the hippocampal tissue of rats in group C were significantly higher than those in group S,while the relevant protein level in group D were significantly lower than those in group C.Conclusion: the above studies showed that SAE can damage the learning and memory function of rats,while diammonium glycyrrhizinate can reduce the level of inflammatory factors and reduce excessive inflammatory response by inhibiting hmgb-1 expression,thus playing a certain therapeutic role in SAE rats. |
PDF Full Text Request