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目的研究瑞舒伐他汀对哮喘小鼠toll样受体4(TLR-4)及其下游炎症因子TNF-α、IFN-γ、IL-4、、IL-5表达的影响。方法采用卵蛋白(OVA)激发BALB/C小鼠的方法建立哮喘模型;将哮喘模型小鼠45只随机分为空白对照组、哮喘组(ova组)、瑞舒伐他汀组(OVA+RUS组),各15只。分别给予OVA、OVA+RUS处理,并于4周后处死大鼠,用ELISA法检测外周血、肺泡灌洗液中TNF-α、IFN-γ、IL-4、、IL-5的表达,并对肺泡灌洗液进行细胞分类计数,用RT-PCR法检测外周血TLR-4基因的转录,用Western blot法检测外周血TLR-4蛋白的表达。结果与哮喘组相比,瑞舒伐他汀组肺泡灌洗液中细胞总数、中性粒细胞总数、嗜酸性粒细胞总数均显著下降,差异有统计学意义(P<0.05);瑞舒伐他汀组TLR-4蛋白的转录及表达显著降低,差异有统计学意义(P<0.01);瑞舒伐他汀组外周血及肺泡灌洗液中TNF-α、IFN-γ、IL-4、、IL-5的表达明显降低,差异有统计学意义(P<0.05);在哮喘组和瑞舒伐他汀组TLR4蛋白的表达水平分别与TNF-α、IFN-γ、IL-4、、IL-5水平呈正相关。结论瑞舒伐他汀能降低OVA诱发哮喘大鼠肺组织TLR-4蛋白的表达,并降低炎症因子TNF-α、IFN-γ、IL-4、、IL-5的表达,其作用机制可能与其抑制TLR-4信号通路有关。
Objective To investigate the effect of rosuvastatin on the expression of toll like receptor 4 (TLR-4) and its downstream inflammatory cytokines TNF-α, IFN-γ, IL-4 and IL-5 in asthmatic mice. Methods BALB / C mice were induced by ovalbumin (OVA) to establish asthma model. 45 asthmatic mice were randomly divided into blank control group, ova group, rosuvastatin group (OVA + RUS group ), Each 15. The rats were sacrificed after 4 weeks, and the expressions of TNF-α, IFN-γ, IL-4 and IL-5 in peripheral blood and BALF were detected by ELISA The bronchoalveolar lavage fluid was collected for cell counting. The transcription of TLR-4 gene in peripheral blood was detected by RT-PCR. The expression of TLR-4 protein in peripheral blood was detected by Western blot. Results Compared with the asthma group, the total number of alveolar lavage fluid, the total number of neutrophils and the total number of eosinophils in rosuvastatin group were significantly decreased, the difference was statistically significant (P <0.05); rosuvastatin The transcription and expression of TLR-4 protein were significantly lower in the rosuvastatin group than in the rosuvastatin group (P <0.01). The levels of TNF-α, IFN-γ, IL-4 and IL- (P <0.05). The expressions of TLR4 protein in asthma group and rosuvastatin group were significantly lower than those in control group The level was positively correlated. Conclusions Rosuvastatin can reduce the expression of TLR-4 protein and decrease the expression of inflammatory cytokines TNF-α, IFN-γ, IL-4 and IL-5 in asthmatic rats induced by OVA TLR-4 signaling pathway.