College of Animal Science & Technology, College of Animal Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070 Hubei, China.
College of Pharmacy, Linyi University, Linyi, 276000 Shandong, China.
Oxid Med Cell Longev. 2022 Jul 5;2022:3541731. doi: 10.1155/2022/3541731. eCollection 2022.
In this study, we evaluated the in vivo effect of arctigenin (ATG) on bleomycin-induced pulmonary fibrosis in mice and assessed the role of antioxidant activity. Hematoxylin and eosin (H&E) staining, the results of Masson's trichrome, and Sirius red staining showed that bleomycin induced obvious pathological changes and collagen deposition in the lung tissue of mice, which were effectively inhibited by ATG. Specifically, based on immunohistochemistry and western blot results, ATG inhibited the expression of fibrosis markers, such as collagen, fibronectin, and -SMA. Moreover, ATG regulated reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) in the lung tissue of pulmonary fibrosis mice and reduced the pressure of oxidative stress. ATG also regulated the TGF--induced expression of p-Akt, confirming that ATG can inhibit fibrosis through antioxidant activity modulation.
在这项研究中，我们评估了牛蒡子苷元（ATG）对博来霉素诱导的小鼠肺纤维化的体内作用，并评估了其抗氧化活性的作用。苏木精和伊红（H&E）染色、马松三色染色和天狼星红染色的结果表明，博来霉素诱导了小鼠肺组织的明显病理变化和胶原沉积，而 ATG 可有效抑制这些变化。具体而言，基于免疫组织化学和 Western blot 结果，ATG 抑制了纤维化标志物（如胶原蛋白、纤维连接蛋白和 -SMA）的表达。此外，ATG 调节了肺纤维化小鼠肺组织中的活性氧（ROS）、超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽（GSH），减轻了氧化应激的压力。ATG 还调节了 TGF-β诱导的 p-Akt 表达，证实 ATG 可以通过抗氧化活性调节来抑制纤维化。
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