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

Treatment of BV2 cells with Micheliolide(MCL) significantly repressed LPS-stimulated nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, as well as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide (NO) induction.?MCL also attenuated mRNA levels of multiple pro-inflammatory cytokines and mediators such as iNOS, COX-2, TNF-α, IL-6 and IL-1β.?Mechanistic studies revealed that MCL suppressed LPS-stimulated the activation of IκBα/NF-κB pathway and Akt pathway.?Moreover, MCL inhibited LPS-induced the activition of c-Jun N-terminal kinase (JNK), p38 MAPK kinase, and extracellular signal-regulated kinases 1/2 (ERK1/2).?Meanwhile, MCL markedly promoted antioxidant protein heme oxygenase-1 (HO-1) expression by enhancing NF-E2-related factor 2 (Nrf2) activity.?Together, ?MCL may serve as a neuroprotective agent in neuroinflammation-related neurodegenerative disorders.

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.