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Effects of triptolide on the expression of MHC II in microglia in kainic acid‑induced epilepsy.

The purpose of the present study was to determine whether triptolide (T10) had any effect on major histocompatibility complex class II (MHC II) expression in kainic acid (KA)‑activated microglia, and to investigate the underlying molecular mechanism. BV‑2 microglia were pretreated with T10 prior to activation with KA. The expression level of MHC II and class II transactivator (CIITA) mRNA was determined via reverse transcription‑polymerase chain reaction. The expression of MHC II, CIITA and the phosphorylation level of c‑Jun and proto‑oncogene c‑Fos (c‑Fos) was determined by western blotting. The protein expression level of MHC II was determined by immunocytochemistry. It was observed that the mRNA and protein levels of MHC II and CIITA were increased in KA‑activated BV‑2 microglia, and that this increase was almost completely eliminated by T10. AP‑1 is a family of homodimers or heterodimers, composed of Jun family and Fos family proteins. Sequence analysis revealed an AP‑1 DNA binding site in the promoter of CIITA. The phosphorylation of c‑Jun and c‑Fos was increased in KA‑activated microglia, while T10 was able to suppress the phosphorylation of c‑Jun and c‑Fos in KA‑activated microglia. These data suggested that T10 may exert suppressive effects on MHC II expression in KA‑activated microglia, and that the mechanism may involve the regulation of AP‑1 activity.