首页|雷公藤甲素通过调控NLRP3通路抑制LPS诱导的BV2小胶质细胞炎性反应

雷公藤甲素通过调控NLRP3通路抑制LPS诱导的BV2小胶质细胞炎性反应

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目的 基于炎症小体(NLRP3)通路探讨雷公藤甲素(Triptolide TP)抑制小胶质细胞炎性反应的机制.方法 脂多糖(LPS)刺激BV2小胶质细胞促细胞炎症损伤,建立体外模型,观察TP对LPS刺激的小胶质细胞的影响.BV2小胶质细胞分为对照组、LPS诱导的模型组(1 mg/L LPS)、TP组(1 nmol/L TP+1 mg/L LPS).对照组不做处理,其它组药物作用24 h,镜下观察药物组细胞发生的形态变化并和对照组比较;细胞上清液用Griess法测定一氧化氮(NO)的释放量;免疫荧光染色和Western blot法检测各组细胞间炎症小体蛋白3(NLRP3)、凋亡相关斑点样蛋白(ASC)、半胱氨酸天冬氨酸蛋白酶(caspase-1)和白细胞介素-18(IL-18)的水平差别.结果 LPS诱导BV2细胞炎性活化,形态呈阿米巴样,降低细胞活性,促进NO的释放.TP作用后降低NO水平,使NLRP3炎性小体激活受到抑制,NLRP3、ASC、caspase-1和IL-18表达水平低下.结论 TP对小胶质细胞炎性反应有抑制作用,发挥了TP的抗炎作用,抑制了NLRP3炎性小体的活化和表达.
Triptolide Inhibits LPS-induced Inflammatory Response in BV2 Microglia by Modulating the NLRP3 Pathway
Objective To investigate the mechanisation of triptolide TP inhibiting microglial inflammation based on the inflam-mosome(NLRP3)pathway.Methods BV2 microglia and lipopolysaccharide(LPS)were selected to stimulate microglia to promote cell inflammatory damage,and an in vitro model was established to observe the effect of TP on LPS-stimulated microglia.The BV2 microglia was divided into three experimental groups:control group,LPS-induced model group(1 μg/mL LPS),and TP group(1 nmol/L TP+1 μg/mL LPS).The control group was not treated,the other groups was treated by the drug for 24 h,then the morpholog-ical changes of the cells in the drug groups were observed by microscope and compared with the control group.Cell supernatants are determined by the Griess method for nitric oxide(NO)release;Immunofluorescence staining and Western blot assays were used to detect the levels of intercellular inflamamite protein 3(NLRP3),apoptosis-associated spot-like protein(ASC),cysteine aspartate pro-tease(caspase-1),and interleukin-18(IL-18).Results LPS-induced inflammatory activation of BV2 cells,which was amoebias-like,reduced cell activity and promoted the release of NO.After TP,it reduces NO levels,inhibits the activation of NLRP3 inflamma-somes,and the expression of the corresponding components NLRP3,ASC,caspase1 and IL-18 was dropped.Conclusion TP has an inhibitory effect on microglial inflammation,exerting its anti-inflammatory effect and inhibiting the activation and expression of NLRP3 inflammasomes.

triptolidelipopolysaccharidesBV2 cellsNLRP3 inflammasomeinflammatory response

穆秉桃、李玉璐、刘淇源、孙肖乐、胡芬琦、曹佳蕾、杨凤君、李佩佩、毕宇锦、王泽涛、张慧宇

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山西大同大学脑科学研究所/分子细胞免疫学大同市重点实验室,山西大同 037009

山西大同大学医学院,山西大同 037009

山西大同大学中医药健康服务学院,山西大同 037009

雷公藤甲素 脂多糖 BV2细胞 NLRP3炎症小体 炎症反应

山西大同大学大学生创新创业训练计划项目山西省基础研究计划项目

XDC202218620210302123478

2024

山西大同大学学报(自然科学版)
山西大同大学

山西大同大学学报(自然科学版)

影响因子:0.271
ISSN:1674-0874
年,卷(期):2024.40(1)
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