雷公藤红素抑制肥大细胞释放IgE及炎症因子的研究

Study on Inhibiting the Release of IgE and Inflammatory Factors from Mast Cells by Tripterine

摘要: 目的：探讨雷公藤红素对肥大细胞IgE及IL-1β、IL-10的抑制作用，旨在为雷公藤红素抑制肥大细胞的作用提供实验室依据。方法：选用18只雄性SD大鼠，并将其分为对照组、模型组以及给药组。模型组通过MCDP刺激诱导肥大细胞脱颗粒；给药组在MCDP刺激后加入雷公藤红素进行处理。通过ELISA法对各组样本的血清IgE进行检测；采用Q-PCR对各组样本的IL-1β、IL-10的mRNA表达水平进行分析。结果：ELISA结果显示，相比对照组，模型组的血清IgE含量有明显上升，而药物组的血清IgE含量明显低于模型组。Q-PCR结果显示，模型组的IL-1β、IL-10的基因表达量分别为(3.83 ± 0.92)、(3.98 ± 0.46)，与对照组的基因表达量相比均明显增加；而药物组的基因表达量则显著低于模型组(P < 0.05)。结论：雷公藤红素能够抑制肥大细胞释放IgE并且抑制IL-1β和IL-10的mRNA表达，提示其具有抑制肥大细胞的作用。

Abstract: Objective: To investigate the inhibitory effect of tripterine on mast cells IgE, IL-1β and IL-10, and to provide laboratory evidence for the inhibitory effect of tripterine on mast cells. Methods: 18 male SD rats were selected and divided into control group, model group and drug administration group. In the model group, mast cell degranulation was induced by MCDP stimulation. The treatment group was treated with tripterine after MCDP stimulation. Serum IgE was detected by ELISA. The mRNA expression levels of IL-1β and IL-10 were analyzed by Q-PCR. Results: ELISA results showed that compared with the control group, the serum IgE content in the model group was significantly increased, while the serum IgE content in the drug group was significantly lower than that in the model group. Q-PCR results showed that the gene expression levels of IL-1β and IL-10 in the model group were (3.83 ± 0.92) and (3.98 ± 0.46), respectively, which were significantly increased compared with the control group. The gene expression in drug group was significantly lower than that in model group (P < 0.05). Conclusion: Tripterine can inhibit the release of IgE from mast cells and the expression of IL-1β and IL-10 mRNA, suggesting that tripterine can inhibit mast cells.