灯盏花素对博来霉素诱导小鼠肺纤维化的保护作用

Protective action of breviscapine against bleomycin-induced lung fibrosis in mice

目的观察灯盏花素对肺纤维化的保护作用,探讨其可能的作用机制。方法观察灯盏花素对体外培养小鼠胚肺成纤维细胞L929增殖、激活及细胞外基质分泌的影响;应用博来霉素诱导小鼠肺纤维化模型,观察灯盏花素对肺纤维化的保护作用。结果灯盏花素体外对小鼠胚肺成纤维细胞L929无直接细胞毒作用,但能抑制TGF-β1促进的增殖、激活及层粘连蛋白(LN)、Ⅰ型胶原(ColⅠ)分泌。体内灯盏花素能抑制博来霉素诱导的小鼠血清TGF-β1升高,阻止博来霉素诱导的小鼠肺脏SOD、POD、CAT降低,并降低肺脏羟脯氨酸、胶原、MDA及TGF-β1含量。结论灯盏花素有肺纤维化保护作用,其机制可能是通过增加抗氧化防御系统和阻止TGF-β信号实现的。

Aim To observe the protective effects of breviscapine against lung fibrosis and investigate its possible mechanism. Methods Effects of breviscapine on cell proliferation, activation and extracellular matrix secretion were examined in mouse embryonic lung fibroblast L929 cells in vitro. The mouse model of bleomycin-induced lung fibrosis was used to assess the protective effect of breviscapine against lung fibrosis. Results In vitro, breviscapine had no cytotoxicity directly on L929 cells, however, it could suppress cell proliferation, activation and secretion of laminin （LN） and collagen Ⅰ （ Col Ⅰ ） induced by transforming growth factor betal （ TGF-β1 ） in L929 cells. In vivo, breviscapine could prevent increase in serum TGF-β1 and decrease in superoxide dismutase （ SOD ）, peroxidase （ POD ） and catalase （CAT） in mice with lung fibrosis caused by bleomycin. In addition, breviscapine was able to reduce pulmonary hydroxyproline, collagen, malondialdehyde （MDA）and TGF-β1 in lung fibrosis mice. Conclusion Breviscapine has protective effect against lung fibrosis and the possible mechanism is to enhance antioxidative defense activities and prevent TGF-β signal.