[关键词]
[摘要]
目的 探讨草质素苷对香烟烟雾所致慢性阻塞性肺疾病(COPD)大鼠治疗作用及主要作用机制。方法 将40只Wistar大鼠随机分为对照组、模型组和草质素苷低、高剂量(50、100 mg/kg)组,除对照组外,其余各组大鼠采用香烟烟熏法制备COPD模型,连续烟熏30 d,并于每日烟熏结束1 h后,对各组大鼠进行ig给药处理。末次给药后24 h,取大鼠左右侧肺组织,采用HE染色观察大鼠左侧部分肺组织病理学变化;取另一份左侧肺组织,制备组织匀浆,试剂盒法检测过氧化氢酶(CAT)、血红素加氧酶(HO-1)、8-羟基脱氧鸟苷(8-OHDG)及髓过氧化物酶(MPO)含量。取右侧肺组织,平均分为4份,采用免疫组化法观察其中嗜酸性粒细胞趋化因子(Eotaxin)、嗜酸性阳离子蛋白(ECP)、巨噬细胞炎性蛋白-1α(MIP-1α)及淀粉样蛋白A (SAA)炎性因子的阳性表达情况,并观察相对表达量。结果 HE染色结果显示,草质素苷低、高剂量组大鼠肺组织中肺泡间隔变薄及炎症细胞浸润等病理变化程度均不及模型组;与模型组比较,草质素苷低、高剂量组大鼠肺组织匀浆中CAT、HO-1含量均显著升高,8-OHDG、MPO含量则均显著降低(P<0.05)。免疫组化检测结果表明,草质素苷低、高剂量组大鼠Eotaxin、ECP、MIP-1α及SAA的阳性表达程度均不及模型组,且蛋白的相对表达量均明显降低(P<0.05)。结论 草质素苷对香烟烟雾所致COPD具有较好的保护作用,主要机制可能与其抗氧化及抗炎活性有关。
[Key word]
[Abstract]
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.
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[基金项目]
陕西省中医管理局中医药科研课题(15-LC064)