{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chu H"],"funding":["NIAID NIH HHS"],"pagination":["2252"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5440393"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonary fibrosis. We found that regardless of the prophylactic or therapeutic treatment, Shenks was able to attenuate BLM-induced-fibrosis in mice, down regulate extracellular matrix genes expression, and reduce collagen production. The aberrantly high Smad3 phosphorylation levels and SBE activity in TGF-β-induced fibroblasts were dramatically decreased as a result of Shenks treatment. At the same time, Shenks was able to increase the expression of antioxid"],"journal":["Scientific reports"],"pubmed_title":["Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress."],"pmcid":["PMC5440393"],"funding_grant_id":["U01 AI090909"],"pubmed_authors":["Cui J","Liu Q","Ma Y","Jiang S","Zhou X","Wang J","Zhao Y","Shi X","Shi Y","Ding W","Zhong Q","Guo G","Chu H","Jin L"],"additional_accession":[]},"is_claimable":false,"name":"Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress.","description":"Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonary fibrosis. We found that regardless of the prophylactic or therapeutic treatment, Shenks was able to attenuate BLM-induced-fibrosis in mice, down regulate extracellular matrix genes expression, and reduce collagen production. The aberrantly high Smad3 phosphorylation levels and SBE activity in TGF-β-induced fibroblasts were dramatically decreased as a result of Shenks treatment. At the same time, Shenks was able to increase the expression of antioxid","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 May","modification":"2025-04-26T11:05:50.831Z","creation":"2019-03-27T02:45:37Z"},"accession":"S-EPMC5440393","cross_references":{"pubmed":["28533545"],"doi":["10.1038/s41598-017-02293-z"]}}