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目的:通过血压平胶囊对自发性高血压大鼠心肌NF-κB及其下游因子影响的研究,从炎性角度探讨该药治疗高血压病可能的作用机制。方法:SHR24只,随机分为模型对照组、依那普利组和血压平组,每组8只,WKY大鼠8只作为正常对照组。自实验第一天起血压平组和依那普利组分别以相应药物灌胃,每天2次,共8周,正常对照组和模型对照组以等量蒸馏水灌胃。每周末测各组血压,第8周末称左室质量,计算左室质量指数,用Western blot法检测NF-κB的蛋白表达水平及ELISA法检测IL-18、MCP-1、IFN-γ炎性因子浓度。结果:(1)收缩压:依那普利组、血压平组均能有效降收缩压,差异无统计学意义(P>0.05)。(2)左室质量、左室质量指数:依那普利组、血压平组均降低,差异无统计学意义(P>0.05)。(3)NF-κB水平:依那普利组、血压平组均降低,血压平组更低(P<0.05)。(4)心肌IL-18、MCP-1、IFN-γ浓度:依那普利组、血压平组IL-18、MCP-1浓度降低,血压平组明显降低(P<0.01);依那普利组、血压平组IFN-γ浓度升高,血压平组明显升高(P<0.01)。结论:血压平胶囊能下调NF-κB信号转导通路的水平,这可能是其有效控制血压和延缓左室肥厚进展的作用机制之一。
OBJECTIVE: To explore the possible mechanism of action of this drug in the treatment of hypertension from the perspective of inflammation through the study of the influence of blood pressure capsule on NF-κB and its downstream factors in spontaneously hypertensive rats. Methods: SHR 24 rats were randomly divided into model control group, enalapril group and blood pressure group, 8 in each group and 8 in WKY rats as normal control group. From the first day of the experiment, the blood pressure level group and the enalapril group were orally administered with the corresponding drugs twice daily for 8 weeks. The normal control group and the model control group were given gavage with equal volume of distilled water. The blood pressure of each group was measured at the end of each weekend, and the left ventricular mass was weighed at the end of the 8th week. The left ventricular mass index was calculated. The protein expression of NF-κB was detected by Western blot and IL-18, MCP-1 and IFN- Factor concentration. Results: (1) systolic pressure: enalapril group, blood pressure group can reduce systolic pressure, the difference was not statistically significant (P> 0.05). (2) Left ventricular mass, left ventricular mass index: enalapril group, blood pressure group were reduced, the difference was not statistically significant (P> 0.05). (3) NF-κB level: In the enalapril group, the blood pressure level group decreased and the blood pressure level group was lower (P <0.05). (4) The concentration of IL-18, MCP-1 and IFN-γ in the myocardium were decreased in the enalapril group and the level of IL-18 and MCP-1 in the blood pressure group were significantly decreased (P <0.01) The concentration of IFN-γ in the Lee group and the blood-pressure group was significantly increased, and the level in the blood-pressure group was significantly increased (P <0.01). Conclusion: SFJ can down-regulate the level of NF-κB signal transduction pathway, which may be one of the mechanisms of its effect in controlling blood pressure and prolonging the progression of left ventricular hypertrophy.