Jing-Si Herbal Tea Suppresses H 2 O 2 -Instigated Inflammation and Apoptosis by Inhibiting Bax and Mitochondrial Cytochrome C Release in HIG-82 Synoviocytes.
Shih-Wen KaoYu-Chun ChangFeng-Huei LinTai-Lung HuangTung-Sheng ChenShinn-Zong LinKuan-Ho LinWei-Wen KuoTsung-Jung HoChih-Yang HuangPublished in: Environmental toxicology (2024)
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 H 2 O 2 -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 H 2 O 2 -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 H 2 O 2 -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 H 2 O 2 , 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 H 2 O 2 -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.
Keyphrases
- oxidative stress
- induced apoptosis
- cell death
- rheumatoid arthritis
- diabetic rats
- cell cycle arrest
- extracellular matrix
- combination therapy
- inflammatory response
- mesenchymal stem cells
- cell therapy
- mass spectrometry
- stem cells
- replacement therapy
- cell proliferation
- drug induced
- heat shock protein
- interstitial lung disease
- idiopathic pulmonary fibrosis
- newly diagnosed
- anti inflammatory