电针对慢性阻塞性肺疾病大鼠肺组织基质金属蛋白酶9及组织金属蛋白酶抑制剂1表达的影响

目的:观察电针对慢性阻塞性肺疾病(COPD)模型大鼠肺组织中基质金属蛋白酶9(MMP-9)及组织金属蛋白酶抑制剂1(TIMP-1)表达的影响,探讨电针保护肺组织的作用机制。方法:将SD大鼠随机分为正常组、模型组、药物组及电针组,每组10只。采用脂多糖器官滴入加烟熏法复制COPD大鼠模型。从造模第8天开始,药物组给予地塞米松注射液(2mg/kg)腹腔注射,1次/d,连续22d;电针组取"太渊""足三里""丰隆"和"太溪",留针20min,1次/d,连续22d。HE染色后在光学显微镜下观察肺组织结构,免疫组化法检测肺组织MMP-9和TIMP-1的表达水平。结果:HE染色结果显示,相对正常、药物和电针组大鼠,模型组大鼠肺组织中呈弥漫性水肿和炎性细胞浸润,其中杯状细胞明显增多,纤维细胞增生。与正常组比较,模型组大鼠肺组织MMP-9及TIMP-1的表达水平升高(P0.05);与模型组比较,电针、药物可降低肺组织中MMP-9及TIMP-1的表达(P0.05);模型组与正常、药物、电针组相比,MMP-9/TIMP-1下降(P0.05);电针组和药物组比较,两者各指标的差异无统计学意义(P0.05)。结论:电针有保护COPD大鼠肺功能的作用,其机制可能与降低肺组织MMP-9和TIMP-1的表达有关。

Effects of Electroacupuncture Intervention on Expression of Pulmonary Metalloproteinase-9 and Tissue Inhibitor-1 Proteins in Rats with Chronic Obstructive Pulmonary Disease

Objective To observe the effect of electroacupuncture(EA)stimulation on the expression of metalloproteinase-9(MMP-9)and tissue inhibitor-1(TIMP-1)in the lung tissue in rats with chronic obstructive pulmonary disease(COPD),so as to reveal its mechanisms in protecting the lung tissue.Methods Forty male SD rats were equally randomized into control,model,medication and EA groups.The COPD model was established by smoke-fumigation method(passive smoking in a closed box)and endotracheal injection of lipopolysaccharide(200μg/100μL)for 30 days.Rats of the medication group were treated by i.p.of dexamethasone acetate injection(2.0mg/kg),once daily for 22 days.EA was applied to LU 9,ST 36,ST 40 and KI 3for 20 min,once daily for 22 days.Pathological changes of the pulmonary tissue were observed under optical microscope after hematoxylin and eosin(H.E.)staining.The expression of pulmonary MMP-9and TIMP-1was assayed by immunohistochemistry.Results H.E.staining showed pulmonary diffuse edema,severe inflammatory cell infiltration,and increase of the numbers of goblet cells,proliferation of fibroblasts,etc.in the model group which were relatively milder in the medication and EA groups.The expression levels of pulmonary MMP-9and TIMP-1proteins were significantly higher in the model group than in the control group(P<0.05),and were considerably down-regulated in both EA and medication groups in comparison with the model group(P<0.05).There were no significant differences between the EA and medication groups in MMP-9and TIMP-1expression levels(P>0.05).Conclusion EA can effectively suppress the increased expression of pulmonary MMP-9and TIMP-1in COPD rats,which may contribute to its effect in improving COPD-induced pathological changes.