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背景:中医药防治慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)的有效性和安全性已初步得到临床认证。目的:观察COPD模型大鼠肺组织中基质金属蛋白酶9及其特异性抑制物组织金属蛋白酶抑制剂1表达与固本颗粒胶囊干预的影响。方法:将50只Wistar大鼠随机等分为5组,除正常组外,其余大鼠均以烟熏及气管内滴注脂多糖的方式建立COPD模型。造模29d,泼尼松组、固本颗粒胶囊低、高剂量组分别灌胃给予醋酸泼尼松1.04mg/(kg·d),固本颗粒胶囊0.47,0.94g/(kg·d),1次/d,观察记录大鼠的一般状况。免疫组织化学方法检测大鼠肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达。结果与结论:COPD大鼠肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达显著增强(P<0.05)。药物干预后,COPD大鼠的一般状况明显改善,肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达有所降低;其中,醋酸泼尼松的作用最为显著,固本颗粒高剂量次之,低剂量最弱。说明固本颗粒胶囊能以剂量依赖的方式缓解COPD大鼠的临床表现,改善气道重塑,纠正COPD大鼠体内蛋白酶和抗蛋白酶失衡。
BACKGROUND: The effectiveness and safety of traditional Chinese medicine in the prevention and treatment of chronic obstructive pulmonary disease (COPD) have been initially clinically verified. OBJECTIVE: To observe the effect of Guben Capsule on the expression of tissue inhibitor of matrix metalloproteinase-9 and its inhibitor of metalloproteinase-1 in lung tissue of COPD model rats. Methods: Fifty Wistar rats were equally divided into five groups. Except the normal group, all the other rats were given COPD model with smoke and intratracheal instillation of lipopolysaccharide. At the 29th day after modeling, prednisone group and Guben capsule were administrated with 1.04mg / (kg · d) of prednisone acetate and 0.47,0.94g / (kg · d) of Guben capsule respectively, 1 times / d, observed and recorded the general condition of rats. Immunohistochemistry was used to detect the expression of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 in rat lung tissue. RESULTS AND CONCLUSION: The expression of MMP-9 and TIMP-1 in the lung tissue of COPD rats was significantly increased (P <0.05). After drug intervention, the general condition of COPD rats was significantly improved, and the expression of MMP-9 and TIMP-1 decreased in lung tissue. Among them, prednisone acetate had the most significant effect, The lowest dose is the weakest. This shows that Guben capsule can relieve the clinical manifestations of COPD rats in a dose-dependent manner, improve airway remodeling, and correct the imbalance of protease and protease in COPD rats.