葛根素对LPS诱导急性脑损伤小鼠的保护作用

目的:研究葛根素(Pur)对脂多糖(LPS)诱导的小鼠急性感染性脑损伤的保护作用及机制。方法:36只清洁级雄性ICR小鼠随机分为正常对照组(NS)、LPS感染组(LPS)和葛根素组(Pur+LPS)。LPS腹腔注射建立急性脑损伤模型,立即腹腔注射给予葛根素注射液治疗,6和24h后旷场。暗场实验检测各组小鼠的自发活动,WesternBlot检测脑组织白细胞分化抗原14(CD14)和环氧化酶2(C0X-2)蛋白表达量,Nisl染色观察神经元存活情况。结果:与NS组相比,LPS组6和24 h旷场实验自主活动距离和穿格次数显著减少,海马神经元的存活数目显著减少,脑组织CD14和C0X-2蛋白表达量显著升高(P<0.05);与LPS组比较,Pur+LPS组6和24 h时海马神经元的存活率明显提高,且CD14和C0X-2蛋白表达量明显下降(P<0.05)。结论:葛根素注射液对LPS所致小鼠急性感染性脑损伤具有一定保护作用,其作用机制可能与抑制脑组织CD14和C0X-2表达有关。

Protective effects of puerarin on lipopolysaccharide-induced brain injury in mice

Objective:To investigate the influence of puerarin Pur on acute brain inflammation induced by lipopo-lysaccharide(LPS)in mice and the underlying mechanism.Methods:Thirty six male ICR mice were randomly divided into normal group(NS)and lipopolysaccharide(LPS)group and puerarin(Pur+LPS)group.The mice were intraper-itoneally injected with LPS to prepare the infectious acute brain injury model.Puerarin were administered intraperitone-ally immediately after LPS injection.At 6 h and 24 h after puerartin administration,open field test and dark field test were used to analyze the change of locomotor activity.Cluster of differentiation 14(CD14)and Cyelooxygenase-2(COX-2)protein expression of brain tissue in each group were detected by Western Blot and the survival of neurons in hippocampus were determined by means of Nissl staining.Results:At6 h and 24 h after LPS injection,moving dis-tanceand and line crossings in open field test decreased and the number of survival neurons in hippocampus reduced sig-nificantly in LPS group compared with those of control group(P<0.05).Expression of CD14 and COX-2 also inereased significantly in LPS group.After treatment with peurarin,the number of survival neurons in hippocampus inereased significantly.The expression of CD14 and C0X-2 decreased significantly compared with those of LPS group.(P<0.05).Conclusion:Peurarin can attenuate the acute infectious brain injury of mice induced by LPS which is related with inhibiting the CD14 activation and reducing the expression of COX-2.