摘要
为探讨人参皂苷Rb1对Aβ1-42所致小鼠脑片微管相关蛋白(Tau)异常磷酸化的抑制作用及其可能机制,采用Aβ1-42诱导小鼠海马脑片建立Tau蛋白过度磷酸化模型,运用免疫印迹方法观察人参皂苷Rb1对Aβ1-42导致小鼠脑片p-Tau、p-Erk1/2、Erk1/2蛋白水平的影响。实验结果显示,模型组p-Tau、p-Erk1/2表达水平明显高于空白对照组(P<0.01);与模型组比较,人参皂苷Rb1各剂量组p-Tau、p-Erk1/2表达水平显著性降低(P<0.01或P<0.05),且大、中剂量组优于小剂量组;人参皂苷Rb1呈一定的剂量依赖性下调Aβ1-42导致的p-Tau、p-Erk1/2的蛋白水平。本研究表明,人参皂苷Rb1可能通过抑制Erk1/2的激活逆转Aβ1-42所导致的Tau蛋白水平的升高来减少神经纤维缠结。
To observe the effects and the possible mechanisms of ginsenoside Rb1 on abnormal phosphorylation of Tau induced by Aβ1-42 in the hippocampal slices.Slices were divided into model group(treated with Aβ1-42),ginsenoside Rb1 group(treated with Aβ1-42 and different doses of ginsenoside Rb1) and control group(treated with the same volume of vehicle).The expressions of Tau,p-Tau,Erk1/2 and p-Erk1/2 were observed by Western blot.Results showed that the expressions of p-Tau(199,202,396) and p-Erk1/2 in the model group were significantly higher than those in the control group(P<0.01).While,the expressions of p-Tau(199,202,396) and p-Erk1/2 in ginsenoside Rb1 treated groups were significantly lower than those in model group(P<0.01 or P<0.05),and ginsenoside Rb1 showed a dose-dependent reverse effects of p-Tau and p-Erk1/2 expression.The results suggested that ginsenoside Rb1 could reverse Aβ1-42 induced hyperphosphorylation of tau and the mechanism maybe through inhibiting the activation of Erk1/2.
作者
杨淑达
于浩飞
张兰春
李媛
耿艺娟
张荣平
胡炜彦
YANG Shu-da;YU Hao-fei;ZHANG Lan-chun;LI Yuan;GENG Yi-juan;ZHANG Rong-ping;HU Wei-yan(School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products,Kunming Medical University,Kunming 650500,China)
出处
《天然产物研究与开发》
CAS
CSCD
北大核心
2020年第7期1143-1147,1098,共6页
Natural Product Research and Development
基金
国家自然科学基金(81960666,81860254)
云南省创新团队(2020HC008)
云南省科技厅项目(2019FC033)
云南省高层次人才培养支持计划—云岭学者项目。
