國家衛生研究院 NHRI:Item 3990099045/16158

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Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/16158

Title:	Jing-si herbal tea suppresses H2O2-instigated inflammation and apoptosis by inhibiting bax and mitochondrial cytochrome C release in HIG-82 synoviocytes
Authors:	Kao, SW;Chang, YC;Lin, FH;Huang, TL;Chen, TS;Lin, SZ;Lin, KH;Kuo, WW;Ho, TJ;Huang, CY
Contributors:	Institute of Biomedical Engineering and Nanomedicine
Abstract:	Inflammation is an intrinsic protective mechanism against various forms of cellular injuries in humans; however, its undesired activation results in tissue damage and cell death. The onset of chronic inflammation and oxidative stress are the key characteristics of autoimmune inflammatory diseases such as rheumatoid arthritis (RA), for which an effective treatment is yet to be developed. Therefore, in this study, we investigated the protective effects and molecular mechanisms of a novel herbal preparation, Jing-Si herbal tea (JS), against H2O2-induced inflammation and cellular damage in HIG-82 synoviocytes. We found that JS did not show any significant alterations in cell viability at <188 μg/mL; however, a cytotoxic effect was observed at 188–1883 μg/mL concentrations tested. We found that expressions of inflammation associated extracellular matrix (ECM)-degrading proteases MMP-13, ADAMTS-2, -8, and -17 were abnormally enhanced under H2O2-induced pathological oxidative stress (ROS) in HIG-82 cells. Interestingly, JS treatment not only reduced the ROS levels but also significantly repressed the protein expressions of collagen degrading proteases in a dose-dependent manner. Treatment with JS showed enhanced cell viability against H2O2-induced toxic ROS levels. The expressions of cell protective aggrecan, Collagen II, and Bcl-2 were increased, whereas MMP-13, ADAMTS-2, Cytochrome C, and cleaved Caspase 3 were decreased by JS under inflammatory agents H2O2, MIA, LPS, and TNF-α treatment, respectively, in HIG-82 cells. Interestingly, the cytoprotective effect of JS treatment was attributed to a decreased mitochondrial localization of Bax and a reduction of Cytochrome C release into the cytoplasm of H2O2-treated HIG-82 cells. Collectively, our results suggest a novel protective mechanism of JS for RA treatment, which could be potentially applied as a complementary treatment or as an alternative therapeutic approach to mitigate inflammatory diseases.
Date:	2024-09-05
Relation:	Environmental Toxicology. 2024 Sep 05;Article in Press.
Link to:	http://dx.doi.org/10.1002/tox.24406
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1520-4081&DestApp=IC2JCR
Cited Times(Scopus):	https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85203295587
Appears in Collections:	[Feng-Huei Lin] Periodical Articles

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