目的 探討草質(zhì)素苷對(duì)香煙煙霧所致慢性阻塞性肺疾病（COPD）大鼠治療作用及主要作用機(jī)制。方法 將40只Wistar大鼠隨機(jī)分為對(duì)照組、模型組和草質(zhì)素苷低、高劑量（50、100 mg/kg）組，除對(duì)照組外，其余各組大鼠采用香煙煙熏法制備COPD模型，連續(xù)煙熏30 d，并于每日煙熏結(jié)束1 h后，對(duì)各組大鼠進(jìn)行ig給藥處理。末次給藥后24 h，取大鼠左右側(cè)肺組織，采用HE染色觀察大鼠左側(cè)部分肺組織病理學(xué)變化；取另一份左側(cè)肺組織，制備組織勻漿，試劑盒法檢測(cè)過氧化氫酶（CAT）、血紅素加氧酶（HO-1）、8-羥基脫氧鳥苷（8-OHDG）及髓過氧化物酶（MPO）含量。取右側(cè)肺組織，平均分為4份，采用免疫組化法觀察其中嗜酸性粒細(xì)胞趨化因子（Eotaxin）、嗜酸性陽離子蛋白（ECP）、巨噬細(xì)胞炎性蛋白-1α（MIP-1α）及淀粉樣蛋白A （SAA）炎性因子的陽性表達(dá)情況，并觀察相對(duì)表達(dá)量。結(jié)果 HE染色結(jié)果顯示，草質(zhì)素苷低、高劑量組大鼠肺組織中肺泡間隔變薄及炎癥細(xì)胞浸潤(rùn)等病理變化程度均不及模型組；與模型組比較，草質(zhì)素苷低、高劑量組大鼠肺組織勻漿中CAT、HO-1含量均顯著升高，8-OHDG、MPO含量則均顯著降低（P<0.05）。免疫組化檢測(cè)結(jié)果表明，草質(zhì)素苷低、高劑量組大鼠Eotaxin、ECP、MIP-1α及SAA的陽性表達(dá)程度均不及模型組，且蛋白的相對(duì)表達(dá)量均明顯降低（P<0.05）。結(jié)論 草質(zhì)素苷對(duì)香煙煙霧所致COPD具有較好的保護(hù)作用，主要機(jī)制可能與其抗氧化及抗炎活性有關(guān)。

Objective To study the protective effects and primary mechanisms of rhodionin in the cigarette smoke induced chronic obstructive pulmonary disease (COPD) in rats.Methods Totally 40 Wistar rats were randomly divided into control group,model group,rhodionin low and high dose (50 and 100 mg/kg) group.The method of cigarette smoke was used to establish the model in the groups except control groupfor consecutive 30 d.The low dose group and high dose group were treated by rhodionin with the dose of 50 mg/kg and 100 mg/kg and other groups were treated by saline everyday 1 h after the cigarette smoke was given.The lung were obtained in the groups 24 h after the last treatment.Then the histopathological changes in part of left lung in the rats were observed by HE staining.The tissue homogenate of other part of left lung was performed;The levels of catalase (CAT),heme oxygenase (HO-1),8-hydroxydeoxyguanosine (8-OHDG) and myeloperoxidase (MPO) were detected.The right lung was divided into four parts and the immunohistochemistry was performed to observe the expression of eotaxin,eosinophilic cationic protein (ECP),macrophage inflammatory protein-1(MIP-1α) and amyloid protein A (SAA) and the relative transcript levels of those proteins were observed.Results Histopathological results showed that the alveolar septum thinning and inflammatory cell infiltration in low dose group and high dose group were significantly improved than model group.Compared with the model group,the levels of CAT and HO-1 were significantly increased,while 8-OHDG and MPO levels were significantly decreased in high dose group and low dose group (P<0.05).Immunohistochemical staining indicated that,compared with the model group,the positive expression of eotaxin,ECP,MIP-1α and SAA in high dose group and low dose group were significantly lower (P<0.05).The results of semi-quantitative analysis show that,the relative transcript levels of eotaxin,ECP,MIP-1α and SAA in high dose group and low dose group were significantly lower than model group (P<0.05).Conclusion Rhodionin could promote the cigarette smoke induced chronic obstructive pulmonary disease in rats and the primary mechanism may be the effect of the compound has good anti-oxidant and antiinflammatory activities.

陜西省中醫(yī)管理局中醫(yī)藥科研課題（15-LC064）