李探,徐宏彬,张潇月,邵龙刚,刘克琴

• 1:江苏省第二中医院

摘要(Abstract)：

目的 探讨没药甾酮（GS）下调Toll样受体4(TLR4)/核转录因子-κB(NF-κB)通路减轻脓毒症相关性脑病（SAE）神经炎症反应的机制。方法 采用脂多糖（LPS）诱导小鼠小胶质细胞系（BV2细胞）制备脓毒症相关性脑病细胞模型。在此细胞模型中，通过CCK-8法检测BV2细胞的增殖凋亡情况，确定LPS和GS的最佳给药浓度；在此给药浓度基础上分为空白对照组（NC组）、LPS组及LPS+GS组，采用Western blotting法检测给药6、12、24 h后TLR4/NF-κB通路关键蛋白的表达情况；最后，采用ELISA法检测细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、转化生长因子-β(TGF-β)、白细胞介素-10(IL-10)的表达情况。结果 当LPS浓度≥3μg/mL和GS浓度>30μg/mL时细胞增殖被显著抑制（P <0.01），选择LPS(3μg/mL)和GS(30μg/mL)作为联合给药浓度，在此浓度基础上联合给药最长至168 h,BV2细胞增殖仍稳定，故选择此浓度作为最佳给药浓度。与NC组相比，LPS诱导后各时间点TLR4/NF-κB通路蛋白表达均有不同程度的增加，差异有统计学意义（P <0.05）。LPS诱导后，促炎细胞因子TNF-α、IL-1β表达较NC组显著增加（P <0.05）；与LPS组相比，GS干预后能在一定程度上下调TNF-α、IL-1β表达，并上调TGF-β、IL-10的表达，差异有统计学意义（P <0.05）。结论 在LPS诱导的SAE细胞模型中，炎症通路TLR4/NF-κB被激活，没药甾酮能够下调此通路关键蛋白的表达，减轻脓毒症相关性脑病神经炎症反应。

关键词(KeyWords)： 脓毒症相关性脑病;没药甾酮;神经炎症反应;脂多糖;BV2细胞;TLR4/NF-κB通路

Abstract:

Keywords:

基金项目(Foundation): 江苏省第二中医院院内课题重点项目（SEZ2019007）;; 南京中医药大学自然科学基金项目（XZR2020052）

作者(Author): 李探,徐宏彬,张潇月,邵龙刚,刘克琴

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