Inhibitory effects of total ginsenoside on bleomycin-induced pulmonary fibrosis in mice
Inhibitory effects of total ginsenoside on bleomycin-induced pulmonary fibrosis in mice
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人参总皂苷对博莱霉素诱导的小鼠肺纤维化的抑制作用
DOI：
10.1016/j.biopha.2019.108851
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发表时间：
2019
影响因子：
7.5
通讯作者：
Deng Jiang
中科院分区：
文献类型：
--
作者：
Yang Lu;Chen Pan pan;Luo Min;Shi Wan lan;Hou Dong shun;Gao Yang;Xu Shang fu;Deng Jiang
肺纤维化是多种弥漫性肺间质性疾病的最终结局，其发病机制尚不清楚。目前尚无有效药物治疗，临床预后较差。人参总皂苷（TG）作为人参的有效成分，具有抑制急性肺损伤的作用。本研究确定TG是否对肺纤维化具有保护作用并探讨其保护机制。通过气管注射博莱霉素化疗剂建立BALB/c小鼠肺纤维化模型。从模型建立后的第二天开始连续给予TG（40、80和160mg/kg/d）28天。通过测量肺系数、苏木精和伊红以及肺样本的马森三色染色，并检测肺组织中α平滑肌肌动蛋白的表达来确定肺纤维化。为了探讨TG抗肺纤维化的机制，我们检测了转化生长因子-β1（TGF-β1）/Smad信号通路和基质金属蛋白酶（MMP）系统的基因和蛋白。 TG（40、80和160mg/kg/d）治疗可改善博莱霉素诱导的小鼠肺纤维化，下调TGF-β1、Smad2、Smad3、MMP-2、MMP-9和金属蛋白酶组织抑制剂1的表达，并上调Smad7的蛋白表达。这些结果提示TG对博来霉素诱导的肺纤维化的保护作用与调节TGF-β1/Smad信号通路和MMP系统有关。
Pulmonary fibrosis is the final outcome of a variety of diffuse pulmonary interstitial diseases, and it has an unclear pathogenesis. There is no effective drug treatment, so the clinical prognosis is poor. As an effective component of ginseng, total ginsenoside (TG) inhibits acute lung injury. This study determined whether TG has protective effects on pulmonary fibrosis and investigated its protective mechanisms. A pulmonary fibrosis model in BALB/c mice was established by injecting the bleomycin chemotherapeutic agent into the trachea. TG (40, 80, and 160 mg/kg/d) was given continuously for 28 days from the second day after development of the model. Pulmonary fibrosis was determined by measuring the lung coefficient, haematoxylin and eosin, and Masson’s trichrome staining of lung samples, and detection of alpha smooth muscle actin expression in lung tissues. To investigate the mechanisms of anti-pulmonary fibrosis by TG, we detected the genes and proteins of the transforming growth factor-β1 (TGF-β1)/Smad signalling pathway and matrix metalloproteinase (MMP) system. Treatment with TG (40, 80, and 160 mg/kg/d) ameliorated pulmonary fibrosis induced by bleomycin in mice, downregulated the expression of TGF-β1, Smad2, Smad3, MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1, and upregulated the protein expression of Smad7. These results suggest that the protective effects of TG on pulmonary fibrosis induced by bleomycin are related to regulation of the TGF-β1/Smad signalling pathway and MMP system.