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目的研究氟伐他汀抑制干扰素-γ(IFN-γ)诱导的内皮细胞表面主要组织相容性抗原复合物Ⅱ(MHCⅡ)表达的作用,并研究其抑制作用的机理。方法通过流式细胞仪检测分析MHCⅡ在内皮细胞中的表达,通过RT-PCR检测Ⅱ类反式激活因子(CⅡTA)mRNA的生成,通过Western blot分析信号转导和转录激活因子1(STAT1)的总量和磷酸化STAT1(P-STAT1)。结果氟伐他汀预处理可以抑制由IFN-γ刺激诱导的内皮细胞表面MHCⅡ表达,RT-PCR分析表明CⅡTA mRNA的诱导生成可以被氟伐他汀阻断。Western blot分析表明氟伐他汀预处理并不影响STAT1的总量和在IFN-γ刺激后STAT1的磷酸化。结论在内皮细胞中,氟伐他汀预处理可以抑制由IFN-γ刺激诱导的CⅡTA mR- NA的表达,并因此抑制了细胞表面MHCⅡ表达,这种抑制作用主要发生在CⅡTA的转录水平,可能与转录因子和CⅡTA启动子的结合有关。
Objective To investigate the inhibitory effect of fluvastatin on the expression of major histocompatibility complex antigen Ⅱ (MHC Ⅱ) on the surface of endothelial cells induced by interferon-γ (IFN-γ) and its mechanism of inhibition. Methods The expression of MHCⅡ in endothelial cells was detected by flow cytometry. The generation of class Ⅱ transactivator (CⅡTA) mRNA was detected by RT-PCR. The expression of signal transducer and activator of transcription 1 (STAT1) Total and phosphorylated STAT1 (P-STAT1). Results Fluvastatin pretreatment inhibited the expression of MHCⅡ on the surface of endothelial cells stimulated by IFN-γ. RT-PCR analysis showed that the induction of CⅡTA mRNA could be blocked by fluvastatin. Western blot analysis showed that fluvastatin pretreatment did not affect the total amount of STAT1 and phosphorylation of STAT1 after IFN-γ stimulation. Conclusions In endothelial cells, fluvastatin pretreatment can inhibit the expression of CⅡTA mR-NA induced by IFN-γ, and thus inhibit the expression of MHCⅡ on the cell surface. This inhibition mainly occurs at the transcription level of CⅡTA, which may be related to The transcription factor is involved in the binding of the C II TA promoter.