益气活血通络法对COPD大鼠肺血管重构的影响

    Effect of Tonifying Qi, Promoting Blood Flow and Dredging Collaterals Treatment on Pulmonary Vascular Remodeling of COPD Rats

    • 摘要: 目的 观察益气活血通络法对慢性阻塞性肺疾病(chronic obstructive pulmonary diseases,COPD)大鼠肺血管重构IL-6/JAK/STAT信号转导通路的影响。方法 SD大鼠50只,随机均分为正常对照组、模型组、中药组、西药组和中西医结合组。采用气道滴注脂多糖联合香烟烟雾暴露的方法制备大鼠COPD肺血管重构模型。药物干预后各组大鼠右下肺叶行HE染色观察肺血管病理形态学变化,并采用ELISA法检测血清IL-6含量变化; Western blot测定肺组织p-JAK2和p-STAT3蛋白表达水平;免疫组化技术检测肺动脉增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)蛋白表达。结果 与模型组比较,各药物组大鼠血清IL-6含量及肺动脉PCNA表达显著减少(P<0.05或<0.01),p-JAK2和p-STAT3表达显著降低(P均<0.01);中西医结合组较中药组及西药组p-JAK2表达均显著下降(P均<0.01)。结论 中医益气活血通络法能有效减轻COPD大鼠肺血管重构,其机制可能与抑制IL-6/JAK/STAT信号转导通路进而调节肺小动脉PCNA表达有关。

       

      Abstract: OBJECTIVE To observe the effects of tonifying Qi, promoting blood flow and dredging collaterals treatment on IL-6/JAK/STAT signaling pathway of pulmonary vascular remodeling of COPD rats. METHODS Fifty SD rats were randomly divided into normal control group, model group, Chinese medicine group, western medicine group, and integrated Chinese and western medicine group. The rat model of COPD was established by intratracheal instillation of LPS and daily exposure to cigarette-smoking. The pathological features of pulmonary arteries were observed by microscope after intervention of drugs. The serum contents of IL-6 was detected by ELISA. The expressions of p-JAK2 and p-STAT3 were detected by Western blot. The content of the protein expression levels of PCNA in pulmonary artery were detected by immunohistochemistry. RESULTS The serum content of IL-6 and protein expression levels of PCNA in each drug group was significantly lower than in model group (P<0.05 or <0.01). P-JAK2 and p-STAT3 expression level in each drug group was significantly lower than in model group (P<0.01). P-JAK2 expression level in integrated Chinese and western medicine group was lower than in Chinese medicine group and western medicine group significantly (P<0.01). CONCLUSION Tonifying Qi, promoting blood flow and dredging collaterals treatment may reduce the remodeling of pulmonary vascular by the way of inhibiting the activation of IL-6/JAK/STAT signal pathway, which can lead to regulate the protein expression levels of PCNA.

       

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