These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Interventional effect of metformin on pulmonary inflammation and pulmonary fibrosis in silicotic rats].
    Author: Li SX, Pang XR, Yan HY, Zhang J, Jia Q, Li C, Shao H, Yu GC.
    Journal: Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi; 2021 Oct 20; 39(10):726-732. PubMed ID: 34727651.
    Abstract:
    Objective: To investigate the interventional effect of metformin on pulmonary inflammation and pulmonary fibrosis in silicotic rats. Methods: In April 2019, 48 Wistar male rats of SPF grade were randomly divided into negative control group, metformin control group, silicon dioxide (SiO2) model group, low, medium and high dose metformin intervention group according to the random number table method, 8 rats in each group. The SiO2 model group and the low, medium and high dose metformin intervention groups were given 1 ml 50 mg/ml of SiO2 by intratracheal instillation, the negative control group and the metformin control group were given 1 ml normal saline by intratracheal instillation. 24 hours later, the low, medium and high dose metformin intervention groups and the metformin control group were treated with 100, 200, 400 and 400 mg/kg metformin daily, the control and SiO2 model groups received normal saline daily. Then the rats were sacrificed at the 28th day after SiO2 exposure. The changes of rat body weight and pathological examination of rat lung tissue were observed, and the lung organ coefficient, the content of hydroxyproline (HYP) , the expression levels of inflammatory factors transforming growth factor beta1 (TGF-β1) , tumor necrosis factor-alpha (TNF-α) , interleukin-1beta (IL-1β) and the protein expression of E-cadherin (E-Cad) , Vimentin, α-SMA were detected. Results: Compared with the negative control group, SiO2 model group had a significant decrease in the body weight of rats (P<0.05) , lung organ coefficient, alveolitis and fibrosis scores, HYP content and the levels of TGF-β1, TNF-α, IL-1β were all significantly increased (P<0.05) . Compared with the SiO2 model group, the weights of the rats in the medium and high dose intervention group of metformin increased significantly (P<0.05) . And after intervention with different doses of metformin, the lung organ coefficient, alveolitis and fibrosis scores, HYP content and the levels of TGF-β1, TNF-α and IL-1β were significantly decreased (P<0.05) . Immunohistochemistry and Western blotting results showed that compared with the negative control group, the expression of E-Cad of the SiO2 model group was decreased, and the expression levels of Vimentin and α-SMA were significantly increased (P<0.05) . After metformin intervention, the expression of E-Cad was significantly increased, the expression levels of Vimentin and α-SMA were significantly decreased (P<0.05) . Conclusion: Metformin can reduce lung tissue inflammation and fibrosis in rats exposed to SiO2 dust, which may be related to reducing the expression of inflammatory factors in lung tissue and inhibiting the EMT process. 目的： 探讨二甲双胍对矽肺大鼠肺炎及肺纤维化的干预作用。 方法： 于2019年4月，将48只SPF级Wistar雄性大鼠按随机数字表法随机分为阴性对照组、二甲双胍对照组、二氧化硅（SiO2）模型组以及二甲双胍低、中、高剂量干预组，每组8只。SiO2模型组和二甲双胍各剂量干预组一次性经气管灌注1 ml 50 mg/ml SiO2，阴性对照组和二甲双胍对照组经气管灌注1 ml生理盐水。染尘24 h后，二甲双胍低、中、高剂量干预组及二甲双胍对照组分别经口灌胃100、200、400、400 mg/kg二甲双胍，阴性对照组和SiO2模型组给予等容积的生理盐水；每天给药1次，连续28 d。染尘28 d后处死大鼠，观察各组大鼠体重变化情况，计算肺系数，观察病理学改变，检测肺组织中羟脯氨酸（HYP）、转化生长因子-β1（TGF-β1）、肿瘤坏死因子α（TNF-α）和白细胞介素1β（IL-1β）的水平以及肺上皮-间质转化（EMT）相关蛋白E-钙黏蛋白（E-Cad）、波形蛋白（Vimentin）、α-平滑肌肌动蛋白（α-SMA）的表达水平。 结果： 与阴性对照组比较，SiO2模型组大鼠体重降低（P<0.05），肺系数、肺泡炎和纤维化评分、HYP含量以及TGF-β1、TNF-α和IL-1β的表达水平均明显升高（P<0.05）；与SiO2模型组比较，二甲双胍中、高剂量干预组大鼠体重明显升高（P<0.05），二甲双胍各剂量干预组肺系数、肺泡炎和纤维化评分、HYP含量以及TGF-β1、TNF-α和IL-1β的表达水平均明显降低（P<0.05）。免疫组化和蛋白免疫印迹结果显示，与阴性对照组比较，SiO2模型组大鼠肺组织E-Cad表达水平降低，Vimentin和α-SMA表达水平升高（P<0.05）；与SiO2模型组比较，二甲双胍各剂量干预组大鼠肺组织中E-Cad表达水平明显升高，Vimentin和α-SMA的表达水平明显降低（P<0.05）。 结论： 二甲双胍能够减轻矽肺大鼠肺组织炎症和纤维化，可能与其降低肺组织炎症因子表达及抑制EMT进程有关。.
    [Abstract] [Full Text] [Related] [New Search]