Arenaria kansuensis attenuates pulmonary fibrosis in mice via the activation of Nrf2 pathway and the inhibition ofNF-kB/TGF-beta1/Smad2/3 pathway

被引:40
|
作者
Cui, Yulei [1 ]
Xin, Huawei [1 ,2 ]
Tao, Yanduo [3 ,4 ,5 ]
Mei, Lijuan [3 ,4 ,5 ]
Wang, Zhen [1 ]
机构
[1] Linyi Univ, Coll Pharm, Linyi, Shandong, Peoples R China
[2] Linyi Univ, Linyi Key Lab Targeted Therapeut & Drug Delivery, Linyi, Shandong, Peoples R China
[3] Chinese Acad Sci, Northwest Inst Plateau Biol, Xining 810008, Qinghai, Peoples R China
[4] Chinese Acad Sci, Key Lab Tibetan Med Res, Xining, Peoples R China
[5] Key Lab Tibetan Med Res Qinghai Prov, Xining, Peoples R China
关键词
Arenaria kansuensis; COVID-19; inflammation; oxidative stress; pulmonary fibrosis; NF-KAPPA-B; SIGNALING DRIVES; GENE-EXPRESSION; BLEOMYCIN; INFLAMMATION; EXTRACT; TARGETS; MODELS; CELL;
D O I
10.1002/ptr.6857
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Pulmonary fibrosis is a key feature of COVID-19, Chinese herbal medicineArenaria kansuensishas been used for curing pulmonary disease and antivirus for a long time and it has the potential against COVID-19. In this work, protective effect ofA. kansuensisethanol extract (AE) on pulmonary fibrosis was evaluated through paraquat (PQ)-induced pulmonary fibrosis animal model. Results showed that AE could significantly improve the survival rate, increase the body weight and reduce the lung index of mice at the raw drug doses of 700 and 350 mg/kg. Histopathological observation results showed that the destruction degree of lung tissue structure in mice was significantly improved with the increase of AE dosage. Collagen deposition in lung interstitium was significantly reduced. The marker protein alpha-SMA involved in PF were significantly inhibited through repressing TGF-beta1/Smads pathway. The degree of inflammatory infiltration was significantly reduced and inflammatory cytokines were significantly inhibited in mice through inhibiting the NF-kB-p65. Besides, oxidant stress level including upregulated ROS and down-regulated SOD and GSH was efficiently improved by AE through upregulation of Nrf2 and downregulation of NOX4. In summary, this study firstly showed that the protective effect of AE on pulmonary fibrosis was partly due to activation of Nrf2 pathway and the inhibition of NF-kB/TGF-beta1/Smad2/3 pathway.
引用
收藏
页码:974 / 986
页数:13
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