Calycosin Ameliorates Bleomycin-Induced Pulmonary Fibrosis via Suppressing Oxidative Stress, Apoptosis, and Enhancing Autophagy

被引:20
作者
Liu, Haoge [1 ]
Bai, Xiaoxu [2 ]
Wei, Wan [3 ]
Li, Zhipeng [1 ]
Zhang, Zhengju [1 ]
Tan, Weili [1 ]
Wei, Bin [1 ]
Zhao, Hantao [1 ]
Jiao, Yang [4 ]
机构
[1] Beijing Univ Chinese Med, Grad Sch, Beijing, Peoples R China
[2] Beijing Univ Chinese Med, Dept Resp, Fangshan Hosp, Beijing, Peoples R China
[3] Beijing Univ Chinese Med, Dept Geratol, Dongfang Hosp, Beijing, Peoples R China
[4] Beijing Univ Chinese Med, Dept Resp, Dongfang Hosp, Beijing, Peoples R China
基金
北京市自然科学基金; 中国国家自然科学基金;
关键词
MODEL; LUNG;
D O I
10.1155/2022/9969729
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Calycosin (CA) is a flavonoid extracted from the root of Astragalus membranaceus and has antioxidant, anti-inflammation, and antiapoptosis properties. The objective of this study was to investigate the efficacy of CA in protecting against pulmonary fibrosis. CA (14 mg/kg) and SB216763 (20 mg/kg) were administrated to bleomycin-induced pulmonary fibrosis mice for 3 weeks. The results concluded that CA alleviated the inflammation and collagen deposition in pulmonary fibrosis. In addition, CA reduced MDA level, enhanced SOD and TAC activities, and increased the activity of the Nrf2/HO-1 pathway. CA also regulated the expressions of apoptosis-related proteins. Moreover, CA enhanced autophagy via upregulating LC3, beclin1, PINK1, and reducing p62. CA also increased expression of LAMP1 and TFEB, and inhibited the release of lysosome enzymes from ruptured lysosomes. These results provide new evidence that CA protects against pulmonary fibrosis through inhibiting oxidative stress and apoptosis. In addition, autophagy abnormality and lysosome dysfunction are restored by CA.
引用
收藏
页数:12
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