摘要
目的探讨β-细辛醚对APP/PS1小鼠神经炎症的影响及分子机制。方法将6月龄APP/PS1小鼠20只随机分为模型组(model)与β-细辛醚组(40mg/kg),每组10只;另取同龄C57BL/6小鼠作为对照组(control)。Morris水迷宫检测各组小鼠的学习与记忆能力;免疫荧光染色检测各组小鼠海马区小胶质细胞标记物Iba-1表达和Aβ_(1-42)沉积;ELISA检测小鼠脑内IL-6、IL-1β及TNF-α水平;Western blot检测脑内NLRP3、ASC及Caspase-1蛋白表达。结果β-细辛醚能够明显缩短小鼠逃避潜伏期,延长在原目标象限停留时间,明显增加穿越平台次数;降低小鼠海马区Iba-1阳性细胞数量;降低脑组织中IL-6、IL-1β及TNF-α表达水平;抑制海马区Aβ_(1-42)沉积;降低小鼠脑组织中NLRP3、ASC及Caspase-1蛋白表达。结论β-细辛醚能够通过抑制APP/PS1小鼠NLRP3/ASC/Caspase-1信号通路活性来抑制小胶质细胞活化导致的神经炎症。
Objective To investigate the effects and its molecular mechanism ofβ-asarum on neuroinflammation in APP/PS1 mice.Methods Twenty 6-month-old APP/PS1 mice were randomly divided into model group andβ-asarone group(40 mg/kg),with 10 mice in each group.C57BL/6 mice of the same age were used as the control group(control).The learning and memory ability of mice were detected by morris water maze.The expression of microglia marker Iba-1 and the deposition of Aβ_(1-42)in the hippocampus of mice was observed by immunofluorescence staining.The levels of IL-6,IL-1βand TNF-αwere detected by ELISA.The expressions of NLRP3,ASC and Caspase-1 in brain were detected by Western blot.Resultsβ-asarum could shorten the escape latency of mice,prolong the residence time in the original target quadrant,and increase the number of platform crossing,decrease the number of Iba-1 positive cells in the hippocampus of mice,decrease the levels of IL-6,IL-1βand TNF-αin brain tissue,inhibite deposition of Aβ_(1-42)in hippocampus,decrease the expressions of NLRP3,ASC and Caspase-1.Conclusionβ-asarone can inhibit microglia-induced neuroinflammation by inhibiting the NLRP3/ASC/Caspase-1 signaling pathway in APP/PS1 mice.
作者
李秋实
李熙东
田步先
陈龙
LI Qiu-shi;LI Xi-dong;TIAN Bu-xian;CHEN Long(Department of Neurology,the First Affiliated Hospital of Jinzhou Medical University,Jinzhou 121012,China;Department of Anesthesiology,the First Affiliated Hospital of Jinzhou Medical University,Jinzhou 121012,China)
出处
《解剖科学进展》
CAS
2023年第2期142-145,共4页
Progress of Anatomical Sciences
基金
锦州医科大学横向科研项目(2021008)
作者简介
通信作者:陈龙