药用植物紫苏基因导入烟草干预大鼠吸烟相关性肺损伤的研究

Intervention to Smoking-Related Lung Injury of SD Rat by Introducing Medical Plants Perilla frutescens (L.) Britt Genes into Tobacco

54只清洁级雄性SD大鼠随机分为健康对照组(CK)、普通烟草组(GT)和新型烟草组(NT),采用烟雾熏吸法构建COPD模型。分别于染毒14、28 d和56 d后,对右肺组织H.E.、Masson和PAS染色发现,实验大鼠逐步呈现出典型的气道炎症和肺气肿,各组的病理学评分依次为1.97±0.30、23.93±0.73和17.43±0.60。ELISA和IHC分析显示,与CK组相比,GT和NT组BALF中IL-8、TNF-α、MMP-9、TIMP-1、MMP-9/TIMP-1以及肺组织中NF-κBP65的水平变化显著(P<0.05);与GT组相比,NT组的上述指标显著降低(P<0.05)。结果表明,导入紫苏基因的新型烟草明显减缓了肺损伤、抑制了异常炎症反应,能够干预大鼠吸烟相关性COPD的进程,这可能与其有益成分调控NF-κB通路有关。

The fifty-four SD rats were randomly divided into three groups：control （CK） ,general tobacco （GT） and new- type tobacco （NT）. The COPD model was duplicated by exposing GT and NT rats to cigarette smoke until 56 days. Pathological changes in lung tissue were analyzed using H. E. , Masson and PAS staining at 14 d,28 d and 56 d, respectively. The obvious COPD features, such as inflammatory cells infiltration, airway remodeling and destroyed alveoli, were ob- served in the smoking rats. Lung injury scores were as follows ： 1.97 ± 0.30 （ CK group） ,23.93±0.73 （ GT group） and 17.43 ± 0.60 （ NT group）. Simultaneously, the levels of IL-8, TNF-α, MMP-9 and TIMP-1 in BALF and NF-KBP65 in lung tissue were detected by ELISA and immunohistochemical method. Compared to CK group ,there was a significant in- crease in their levels in GT and NT groups,but the ratio of MMP-9/TIMP-1 was obviously decreased （P 〈 0.05）. With the extension of exposure time, there were obvious differences in the pathologic changes and abnormal inflammatory re- sponse between NT and GT group （ P 〈 0.05 ）. The results indicated that the new-type tobacco exposure can slow the progression of COPD,which was probably related to the regulation of NF-KB pathway by some beneficial components.