摘要
目的:探讨五味子乙素(Sch B)对帕金森病(PD)模型小鼠NOD样受体蛋白3(NLRP3)信号通路的影响。方法:将30只C57BL/6雄性小鼠随机分为正常组、模型组和Sch B组,每组10只。模型组和Sch B组采用腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)建立PD模型,正常组注射等量生理盐水。除正常组,Sch B组小鼠从造模第1天给予80 mg/(kg·d)Sch B灌胃,模型组和正常组小鼠予以等体积0.5%羧甲基纤维素钠灌胃,连续干预14 d。采用爬杆实验观察小鼠行为学表现,采用免疫荧光染色法检测小鼠黑质区离子钙接头蛋白(Iba-1)表达,采用蛋白质免疫印迹法检测黑质区CD 11b、白细胞介素18(IL-18)、白细胞介素1β(IL-1β)、NLRP3、凋亡相关斑点样蛋白(ASC)、剪切的胱天蛋白酶-1(cleaved-Caspase 1)和N端-Gasdermin D蛋白(GSDMD-N)表达。结果:与正常组比较,模型组小鼠爬杆时间明显延长(P<0.01),Iba-1荧光强度显著增强(P<0.01),CD 11b、IL-18、IL-1β、NLRP3、ASC、cleaved-Caspase 1和GSDMD-N蛋白表达明显增加(P<0.05或P<0.01)。与模型组比较,Sch B组小鼠爬杆时间显著减少,Iba-1荧光强度显著减弱,同时CD 11b、IL-18、IL-1β、NLRP3、ASC、cleaved-Caspase1和GSDMD-N蛋白表达显著减少(P<0.05或P<0.01)。结论:Sch B能够减轻MPTP诱导的PD小鼠神经炎症,这可能与干预NLRP3信号通路有关。
Objective:To investigate the effect of Schisandrin B(Sch B)on the NOD-like receptor protein 3(NLRP3)signaling pathway in a Parkinson's disease(PD)mouse model.Methods:Thirty male C57BL/6 mice were randomly divided into a normal group,a model group,and a Sch B group,with 10 mice in each group.The PD model was established in the model and Sch B groups via intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP),while the normal group received an equivalent volume of normal saline.From the first day of modeling,mice in the Sch B group were administered Sch B(80 mg/kg·d)via gavage,whereas the model and normal groups received an equivalent volume of 0.5%sodium carboxymethylcellulose by gavage for 14 consecutive days.The pole test was used to assess behavioral performance.Immunofluorescence staining was performed to detect the expression of ionized calcium-binding adapter molecule 1(Iba-1)in the substantia nigra.Western blot analysis was conducted to measure the expression of CD 11b,interleukin-18(IL-18),interleukin-1β(IL-1β),NLRP3,apoptosis-associated speck-like protein(ASC),cleaved caspase-1,and N-terminal gasdermin D(GSDMD-N)in the substantia nigra.Results:Compared with the normal group,the model group exhibited a significantly prolonged pole test time(P<0.01),increased Iba-1 fluorescence intensity(P<0.01),and upregulated expression of CD 11b,IL-18,IL-1β,NLRP3,ASC,cleaved caspase-1,and GSDMD-N(P<0.05 or P<0.01).Compared with the model group,the Sch B group showed a significant reduction in pole test time and Iba-1 fluorescence intensity,along with decreased expression of CD 11b,IL-18,IL-1β,NLRP3,ASC,cleaved caspase-1,and GSDMD-N(P<0.05 or P<0.01).Conclusion:Sch B can alleviate neuroinflammation in MPTP-induced PD mice,possibly by modulating the NLRP3 signaling pathway.
作者
贾璐
肖琪
张仲瑾
王青
李彦青
樊慧杰
柴智
马存根
JIA Lu;XIAO Qi;ZHANG Zhongjin;WANG Qing;LI Yanqing;FAN Huijie;CHAI Zhi;MA Cungen(College of Basic Medical Sciences/The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Neurobiology Research Center,Shanxi University of Chinese Medicine,Jinzhong 030619,China)
出处
《世界中医药》
北大核心
2025年第3期424-428,共5页
World Chinese Medicine
基金
国家中医药管理局青年岐黄学者培养项目(国中医药人教函〔2022〕256号)
山西省自然科学基金项目(202203021212341)
山西中医药大学博士科研启动基金项目(2020BK17)
山西中医药大学科技创新能力培育计划项目(2020PY-JC〔Y〕03)。
