ReferenceID 1210

Ameliorative Effects of Arctigenin on Pulmonary Fibrosis Induced by Bleomycin via the Antioxidant Activity

Oxid Med Cell Longev

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 Masso

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Reference Id
1210
Evidence Id
17800
Core Evidence Id
17800
Source Reference Id
2408
Herb2 Reference Id
HBREF003205
Subject Paper Key
HBIN016609_35847593
Pubmed Id
35847593
Doi
10.1155/2022/3541731
Paper Title
Ameliorative Effects of Arctigenin on Pulmonary Fibrosis Induced by Bleomycin via the Antioxidant Activity
Paper Abstract
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 α -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- β -induced expression of p-Akt, confirming that ATG can inhibit fibrosis through antioxidant activity modulation.
Journal
Oxid Med Cell Longev
Publish Year
2022
Experiment Subject
mouse
Experiment Type
Animal & Cell Experiment
Phenotype Related
Pulmonary Fibrosis; Fibrosis
Paper Title Cn
Paper Title En
Ameliorative Effects of Arctigenin on Pulmonary Fibrosis Induced by Bleomycin via the Antioxidant Activity
Bilingual Status
semi_complete