Effects of triptolide on the expression of MHC II in microglia in kainic acidinduced epilepsy.
Mol Med Rep
; 17(6): 8357-8362, 2018 Jun.
Article
en En
| MEDLINE
| ID: mdl-29693706
ABSTRACT
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. BV2 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 transcriptionpolymerase chain reaction. The expression of MHC II, CIITA and the phosphorylation level of cJun and protooncogene cFos (cFos) 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 KAactivated BV2 microglia, and that this increase was almost completely eliminated by T10. AP1 is a family of homodimers or heterodimers, composed of Jun family and Fos family proteins. Sequence analysis revealed an AP1 DNA binding site in the promoter of CIITA. The phosphorylation of cJun and cFos was increased in KAactivated microglia, while T10 was able to suppress the phosphorylation of cJun and cFos in KAactivated microglia. These data suggested that T10 may exert suppressive effects on MHC II expression in KAactivated microglia, and that the mechanism may involve the regulation of AP1 activity.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Fenantrenos
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Antígenos de Histocompatibilidad Clase II
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Expresión Génica
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Microglía
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Diterpenos
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Epilepsia
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Ácido Kaínico
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2018
Tipo del documento:
Article