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 β和IL-10的mRNA表达,提示其具有抑制肥大细胞的作用。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 β and IL-10 mRNA, suggesting that tripterine can
本研究旨在深度剖析长链非编码RNA P53和P21在大鼠动脉粥样硬化模型中的作用及应用潜能。择取60只大鼠,随机平均划分为正常组与粥样硬化组,借由构建大鼠动脉粥样硬化模型,综合运用多种实验技术(如免疫组织化学染色、实时荧光定量PCR、蛋白质印迹法、酶联免疫分析等)及仪器(如彩色多普勒超声诊断仪),对两组中P53和P21的表达状况、调控机制及其与疾病演进的关联予以系统性且全方位的解析。研究成果有望为动脉粥样硬化的诊断与治疗提供新颖且极具价值的靶点与策略。This study aims to deeply analyze the role and application potential of long non-coding RNA P53 and P21 in rat atherosclerosis model. 60 rats were selected and randomly divided into normal group and atherosclerosis group. By constructing rat atherosclerosis model, a variety of experimental techniques (such as immunohistochemistry staining, real-time fluorescence quantitative PCR, protein blotting, enzyme-linked immunosorbent assay, etc.) and instruments (such as color Doppler ultrasound diagnostic instrument) were used to systematically and comprehensively analyze the expression status, regulatory mechanism and relationship between P53 and P21 and disease progression in the two groups. The research results are expected to provide novel and valuable targets and strategies for the diagnosis and treatment of atherosclerosis.
