丹参滴丸调控HMGB1/RAGE信号通路影响冠脉微循环障碍和心肌重构

    Danshen dripping pill affects coronary microvascular dysfunction and myocardial remodeling via regulating HMGB1/RAGE signaling pathway

      摘要
    • 摘要:
      目的 探讨丹参滴丸通过调控高迁移率族蛋白1（high mobility group box 1, HMGB1）/晚期糖基化终末产物受体（receptor for advanced glycation end products, RAGE）信号通路对冠脉微循环障碍（coronary microvascular dysfunction, CMD）和心肌重构的影响。
      方法 将30只SD大鼠随机分为假手术组、模型组和丹参滴丸（Danshen dripping pill, DDP）给药组，每组10只。通过注射月桂酸钠构建冠脉微循环障碍模型，并对DDP给药组进行连续4周的丹参滴丸干预。采用心脏组织病理学检测、ELISA、透射电子显微镜等方法评估DDP对CMD和心肌重构的影响，检测炎症因子和氧化应激相关指标的变化，通过qPCR和Western blot检测HMGB1/RAGE信号通路的变化。
      结果 DDP显著改善了CMD模型大鼠的心肌病理变化。与模型组相比，DDP减少了模型大鼠心肌细胞变性、炎症细胞浸润和纤维化程度，显著抑制了HMGB1和RAGE的mRNA和蛋白表达（均P<0.05），降低炎症因子IL-1β和TNF-α水平（均P<0.01），抑制了心脏组织的氧化应激水平，MDA表达量显著降低（P<0.05），提高了抗氧化酶SOD和GSH-Px的活性（P<0.05）。
      结论 丹参滴丸通过调控HMGB1/RAGE信号通路显著改善了CMD和心肌重构的病理变化，减少了炎症反应和氧化应激，恢复心肌结构和功能，为其在冠心病治疗中的临床应用提供了新的思路和科学依据。

       

      Abstract:
      AIM To investigate the effects of Danshen Dripping Pill (DDP) on coronary microvascular dysfunction (CMD) and myocardial remodeling by regulating the high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) signaling pathway.
      METHODS Thirty SD rats were randomly assigned to sham surgery, model and DDP treatment groups (n=10 per group). CMD models were induced by sodium laurate injection and the treatment group was given 4 weeks of DDP intervention. Cardiac tissue histopathology, ELISA and transmission electron microscopy were used to evaluated the effects of DDP on CMD and myocardial remodeling, and changes in inflammatory factors and oxidative stress-related indicators were measured. We also analyzed the HMGB1/RAGE signaling pathway using qPCR and Western blot.
      RESULTS  DDP significantly improved myocardial pathological changes in CMD model rats and reduced inflammation and oxidative stress levels. Compared with those in the model group, DDP decreased myocardial cell degeneration, inflammatory cell infiltration and fibrosis, significantly down-regulated expressions of HMGB1, RAGE（P<0.05） and related inflammatory factors IL-1β and TNF-α (P<0.01), suppressed oxidative stress in cardiac tissues, reduced MDA expression and enhanced activities of antioxidant enzymes SOD and GSH-Px (P<0.05).
      CONCLUSION  DDP effectively ameliorates pathological changes in CMD and myocardial remodeling by modulating the HMGB1/RAGE signaling pathway, reducing inflammation and oxidative stress and restoring cardiac structure and function. This provides new insights and scientific basis for its clinical application in coronary heart disease treatment.

       

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