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目的:观察雷公藤内酯醇对炎症因子引起的人肾小管上皮细胞(HKC)主要组织相容性II类抗原(class II MHC)、B7共刺激分子及细胞间粘附分子-1(ICAM-1)过量表达的影响.方法:采用干扰素γ(IFN-γ)和肿瘤坏死因子α(TNF-α)联合刺激人肾小管上皮HKC细胞,诱导细胞过度表达class II MHC、B7-1、B7-2和 ICAM-1.同时在细胞培养液中加入不同浓度的雷公藤内酯醇,观察其对上述过程的影响.采用流式细胞术检测细胞内class II MHC、B7-1、B7-2和 ICAM-1等细胞因子的表达,采用逆转录 PCR技术检测ICAM-1 mRNA表达的变化.结果:(1)IFN-γ和TNF-α以能显著上调class II MHC、B7-1、B7-2共刺激分子和ICAM-1在人肾小管上皮细胞中的表达.(2)雷公藤内酯醇剂量依赖性地抑制IFN-γ和TNF-α引起的class II MHC和B7共刺激分子过度表达,但对ICAM-1的过度表达无显著影响.结论:雷公藤内酯醇能抑制炎症因子引起的人肾小管上皮细胞class II MHC和B7共刺激分子过度表达.这也许是雷公藤内酯醇在一些免疫相关性肾脏疾病中的作用机制之一. (责任编辑 韩向晖)
OBJECTIVE: To observe the effects of triptolide on the expression of major histocompatibility class II MHC, B7 costimulatory molecules and intercellular adhesion molecule-1 (ICAM-1) in human renal tubular epithelial cells (HKC) induced by inflammatory cytokines ) Overexpression in human renal tubular epithelial cells.Methods: Human renal tubular epithelial cells (HKCs) were stimulated with interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α) to induce overexpression of class II MHC, B7-1 and B7- 2 and ICAM-1, respectively.Meanwhile, different concentrations of triptolide were added to the cell culture medium to observe the influence of triptolide on the above process.Class II MHC, B7-1, B7-2 and ICAM were detected by flow cytometry 1 and other cytokines, and the changes of ICAM-1 mRNA expression were detected by RT-PCR.Results: (1) IFN-γ and TNF-α could significantly upregulate the expression of class II MHC, B7-1 and B7-2 (2) Triptolide inhibits the over-expression of class II MHC and B7 costimulatory molecules induced by IFN-γ and TNF-α in a dose-dependent manner, but not on the expression of ICAM-1 in human renal tubular epithelial cells. ICAM-1 overexpression had no significant effect.Conclusion: Triptolide can inhibit the inflammation caused by human renal tubular epithelial cell class II MHC and B7 co-stimulatory molecules overexpression.This may be one of the mechanisms of triptolide in some immune-related kidney disease (Reporter Han Xiang Hui)