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目的:观察血塞通注射液降低COPD患者肺动脉高压的临床作用并探讨其可能机制。方法:将22例确诊慢性阻塞性肺疾病患者随机分为常规治疗组和血塞通治疗组,随机抽取11例无肺疾患正常人作为对照组。常规治疗组予支气管扩张剂、抗生素及吸入糖皮质激素,血塞通治疗组在常规治疗基础上加用血塞通针,正常对照组不予任何治疗措施,2周后比较3组肺功能、肺动脉压及血气分析,ELISA法检测血浆磷酸化Erk1/2、磷酸化P38MAPK蛋白表达情况,评价血塞通注射液对慢性阻塞性肺疾病肺动脉高压的影响及与MAPKs信号通路的关系。结果:(1)常规组和血塞通组治疗后肺动脉压、肺功能及血气分析各项指标均较治疗前明显改善,且血塞通组优于常规组(均P<0.05);(2)ELISA结果:血塞通组综合治疗后血浆p-ERK、p-P38表达降低(均P<0.01),常规组无明显差异(P>0.05),两组比较有统计学差异(均P<0.05)。结论:血塞通注射液可能通过抑制P38MAPK、ERK1/2通路,有效地降低COPD患者肺动脉压,改善肺功能。
Objective: To observe the clinical effect of Xuesaitong injection in reducing pulmonary hypertension in patients with COPD and to explore its possible mechanism. Methods: Twenty-two patients with chronic obstructive pulmonary disease were randomly divided into conventional treatment group and Xuesaitong treatment group. Eleven patients with normal lung disease were randomly selected as the control group. Conventional treatment group to bronchodilators, antibiotics and inhaled corticosteroids, Xuesaitong treatment group on the basis of conventional therapy plus Xuesaitong needle, the normal control group without any treatment, two weeks after the comparison of three groups of lung function, Pulmonary arterial pressure and blood gas analysis. The expressions of phosphorylated Erk1 / 2 and phosphorylated P38MAPK protein in plasma were detected by ELISA. The effect of Xuesaitong injection on pulmonary hypertension in chronic obstructive pulmonary disease and its relationship with MAPKs signaling pathway were evaluated. Results: (1) The indexes of pulmonary arterial pressure, pulmonary function and blood gas analysis in conventional group and Xuesaitong group after treatment were significantly improved compared with before treatment, and Xuesaitong group was superior to the conventional group (all P <0.05); (2) ) ELISA results: The plasma levels of p-ERK and p-P38 were decreased in Xuesaitong group (all P <0.01), but there was no significant difference between the two groups (P> 0.05). Conclusion: Xuesaitong injection can effectively reduce pulmonary arterial pressure and improve pulmonary function by inhibiting P38MAPK and ERK1 / 2 pathways.