中文摘要：

目的：探讨培土生金法对COPD大鼠肺组织线粒体功能的影响。方法：选用Wistar雄性大鼠120只，随机分为6组：即COPD模型组、空白对照组、黄芪建中汤组（高、中、低剂量组）、金水宝胶囊组，气管内滴入LPS加烟熏制成COPD模型。COPD模型制备完毕后，各治疗组每天灌胃1次，共8周。实验结束后检测大鼠肺组织线粒体NADH氧化酶、细胞色素氧化酶（CCO）、琥珀酸脱氢酶（SDH）活性以及细胞色素（a、b、c、c1）含量。结果：与空白纽相比，模型组NADH氧化酶、CCO、SDH活性、细胞色素含量明显下降（P〈0．05）；与模型组相比，各治疗组NADH氧化酶、CCO、SDH活性以及Cyta、Cytb、Cytc、Cytcl含量明显升高（P〈0．05），其中以黄芪建中汤高剂量组升高最显著（P〈0，05）。结论：培土生金法的治疗作用明显优于补益肺肾组，能明显提高COPD大鼠肺组织线粒体功能酶的活性，调节COPD能量代谢从而延缓COPD的进程。

英文摘要：

Objective：To discuss the method of reinforcing earth to Strengthen metal on chronic obstructive pulmonary disease in mitochondria function of rat lung tissue. Methods ：120 healthy male Wister rats are randomly divided into 6 groups：COPD model group, normal group, treatment group with Huangqi Jianzhong Decociton（ high, medium and low dose） groups, Jinshuibao capsule control group. COPD animal model was established by smoke inhalations and intratracheal instillations of lipopolysaeeharide in Wister rats. After coping the model of COPD, Huangqi Jianzhong Decoclton（ high, medium and low dose） groups ,Jinshuibao cap- sule control group were given lavage therapy once a day for 8 weeks. After the end of the experiment, radioimmunoassay was used for the determinations of NADH oxidase, CCO, SDH vitalities and the contents of Cyta, Cytb, Cyte and Cytel. Results ： NADH oxi- dase, CCO, SDH vitalities and the contents of Cyta, Cytb, Cytc and Cytcl in the model group were significantly lower than those in the normal group. Compared with the control group, the expression of NADH oxidase, CCO, SDH vitalities and the contents of Cy- ta, Cytb,Cytc and Cytcl were increased significantly in Huangqi Jianzhong Decociton（ high, medium and low dose） groups and Jinshuibao capsule control group. And the high dose group was the most obvious （P 〈 0. 05 ）. Conclusion：The effect of reinforcing earth to strengthen metal is significantly superior to the method of nourishing lung and kidney. It could significantly improve mitochondria enzyme activity of lung tissue in COPD rats by regulating COPD energy metabolism to delay the process of COPD.