白术提取物苍术酮对脂多糖诱导的BV2细胞神经炎性影响及相关机制研究

Effects and mechanism of atractylone from rhizomes of Atractylodes macrocephala Koidzumi in LPS-induced neuro-inflammation in BV2 microglial cells

研究旨在白术提取物苍术酮(AT)对脂多糖(LPS)诱导的BV2细胞抗炎作用,并探讨其相关机制。提取苍术酮并进行结构鉴定;以LPS诱导BV2细胞建立炎症模型;四甲基偶氮唑蓝(MTT)法检测细胞存活率;Griess反应检测细胞上清液中NO水平;ELISA法检测细胞上清中PGE2、IL-6、TNF-α水平;Western Blot法检测COX-2、iNOS、MAPK、NF-κB蛋白表达。结果表明LPS诱导BV2细胞后NO、PGE2、IL-6、TNF-α水平和COX-2及iNOS蛋白表达显著增高,苍术酮预处理后均显著降低。进一步研究表明苍术酮可显著降低LPS诱导BV2细胞ERK、JNK、NF-κB蛋白表达。说明苍术酮能够有效预防LPS诱导BV2细胞神经炎性反应,机制与抑制炎症通路相关。

The research is to investigate the anti-inflammatory effects of atractylone from rhizomes of Atractylodes macrocephala Koidzumi and mechanism by using LPS-induced microglial BV2 cells.Atractylone was extracted and the structure was identified by NMR.MTT assay was used to observe the cell viability.The content of NO in cell supernatant was measured by Griess reagent.The levels of PGE2,IL-6 and TNF-αwere detected by ELISA kits.The intracellular COX-2、iNOS、MAPK、NF-κB expression was assayed by Western blot.According to the results,the levels of NO,PGE2,IL-6 and TNF-αwere significantly increased induced by LPS in the supernatant of BV2 cells,however,significantly decreased by pre-treatment with atractylone.Furthermore,atractylone significantly inhibited the ERK,JNK and NF-κB expression induced by LPS in BV2 cells.It is suggested that atractylone is able to alleviate LPS-induced inflammatory responses through down-regulation of ERK,JNK and NF-κB pathways in BV2 cells.