Micheliolide(MCL) is a sesquiterpene lactone which inhibits various inflammatory response.

Micheliolide (MCL) 处理BV2细胞显著抑制了由脂多糖(LPS)刺激引发的一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达，以及肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和一氧化氮(NO)的诱导。MCL还降低了多种促炎细胞因子和介质的mRNA水平，包括iNOS、COX-2、TNF-α、IL-6和IL-1β。机理研究揭示，MCL通过抑制LPS激活的IκBα/NF-κB通路和Akt通路达到效果。此外，MCL抑制了LPS诱导的c-Jun氨基末端激酶(JNK)、p38 MAPK激酶和细胞外信号调节激酶1/2(ERK1/2)的激活。同时，MCL通过增强NF-E2相关因子2（Nrf2）活性显著促进了抗氧化蛋白血红素氧合酶-1(HO-1)的表达。 综上所述，MCL可以作为一种在神经炎症相关神经退行性疾病中的神经保护剂。

BV2 cells were pretreated with the indicated concentrations of Micheliolide?1 h prior to stimulation with LPS (1 μg/ml) for 6 h and total RNA was extracted using RaPure Total?RNA Kit.Reverse transcription was performed using RevertAid First Strand cDNA Synthesis Kit.?Real-time PCR analysis was performed using SYBR Select Master Mix ?in conjunction with an ABI Prism 7500 Sequence Detection System with the expression of β-actin as the internal control.?The data were analyzed using the ΔΔCT method.?The primers for iNOS, COX-2, TNF-α, IL-1β, IL-6 and β-actin were described as below.