补肺一号方通过TGF-β1/Smad通路抑制慢阻肺大鼠肺纤维化

Tonic Lung of NO.1 Inhibite Pulmonary Fibrosis in COPD Rats through TGF-β1/Smad Pathway

摘要: 目的：熏香烟联合气道内滴注脂多糖(LPS)法制造慢阻肺(COPD)大鼠模型，研究我省名老中医陈志斌教授经验方补肺一号方对COPD大鼠肺纤维化的抑制作用。方法：选择30只3周龄SPF级别SD大鼠随机分为空白组、模型组、补肺一号方低剂量组、补肺一号方中剂量组、补肺一号方高剂量组，其中模型组、中药组给予香烟联合气道内滴注LPS (1 mg/kg)建立COPD模型，低、中、高剂量组分别采用每天灌胃1.5 g/(kg∙d)、3.0 g/(kg∙d)、6.0 g/(kg∙d)干预，空白组、模型组灌胃生理盐水。8周后，HE染色观察大鼠肺组织，Western blot检测肺组织TGF-β1、Smad蛋白表达量。结果：与空白组比较，模型组气道及肺泡破坏严重，肺组织TGF-β1、Smad蛋白显著升高(P < 0.05)；与模型组比较，低、中剂量组气道及肺泡结构恢复正常，TGF-β1、Smad蛋白显著降低(P < 0.05)。结论：补肺一号方能改善COPD大鼠肺组织炎症，这可能与其能抑制TGF-β1/Smad通路，减轻氧化应激及炎症损伤有关。

Abstract: Objective: The rat model of COPD was made by smoking cigarettes combined with airway dripping of lipopolysaccharide (LPS), to investigate the mechanism of inhibition of pulmonary fibrosis in COPD rats of tonic lung of NO.1 by professor Chen Zhibin, a famous old traditional Chinese medicine doctor in our province. Methods: Thirty 3-week-old SPF SD rats were randomly divided into blank group, model group, low/medium/high-dose groups. Model group and medicine groups were given cigarette combined with LPS (1 mg/kg) to establish COPD model. Medicine groups were given 1.5 g/(kg∙d), 3.0 g/(kg∙d) and 6.0 g/(kg∙d). Blank group and model group were given physiological saline. After 8 weeks, lung tissues of rats were observed by HE, and the expression levels of TGF-β1 and Smad proteins in lung tissues were detected by Western blot. Results: Contrast to the blank group, the airway and alveolar in model group were notably breaked, and TGF-β1 and Smad proteins in lung tissues were remarkably enhanced (P < 0.05). Contrast to model group, the airway and alveolar in low and medium dose groups were back to regular, while TGF-β1 and Smad proteins were remarkably reduced (P < 0.05). Conclusion: Tonic lung of NO.1 can improve lung inflammation in COPD rats, associated with the restrain of TGF-β1/Smad pathway and the reduction of oxidative stress and lesions.