2. Academic Validation
  3. Jing-Si Herbal Tea Suppresses H2O2-Instigated Inflammation and Apoptosis by Inhibiting Bax and Mitochondrial Cytochrome C Release in HIG-82 Synoviocytes

Jing-Si Herbal Tea Suppresses H2O2-Instigated Inflammation and Apoptosis by Inhibiting Bax and Mitochondrial Cytochrome C Release in HIG-82 Synoviocytes

  • Environ Toxicol. 2024 Sep 5. doi: 10.1002/tox.24406.
Shih-Wen Kao 1 2,  Yu-Chun Chang 3 4,  Feng-Huei Lin 5 6,  Tai-Lung Huang 7,  Tung-Sheng Chen 8,  Shinn-Zong Lin 9 10,  Kuan-Ho Lin 11 12,  Wei-Wen Kuo 3 13 14,  Tsung-Jung Ho 15 16 17,  Chih-Yang Huang 4 18 19
Affiliations

Affiliations

  • 1 Graduate Institute of Aging Medicine, China Medical University, Taichung, Taiwan.
  • 2 Department of Orthopedic Surgery, Chung-Shan Medical University Hospital, Taichung, Taiwan.
  • 3 Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung, Taiwan.
  • 4 Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • 5 Institute of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, Taipei, Taiwan.
  • 6 Division of Biomedical Engineering and Nanomedicine Research, National Health Research Institute, Miaoli, Taiwan.
  • 7 Department of Orthopedics, Chung-Kang Branch, Cheng Ching General Hospital, Taichung, Taiwan.
  • 8 School of Life Science, National Taiwan Normal University, Taipei, Taiwan.
  • 9 Department of Neurosurgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • 10 Bioinnovation Center, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • 11 Department of Emergency Medicine, China Medical University Hospital, Taichung, Taiwan.
  • 12 College of Medicine, China Medical University, Taichung, Taiwan.
  • 13 Ph.D. Program for Biotechnology Industry, China Medical University, Taichung, Taiwan.
  • 14 School of Pharmacy, China Medical University, Taichung, Taiwan.
  • 15 School of Post-Baccalaureate Chinese Medicine, College of Medicine, Tzu chi University, Hualien, Taiwan.
  • 16 Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan.
  • 17 Integration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • 18 Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
  • 19 Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.
PMID: 39234996 DOI: 10.1002/tox.24406
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.

Keywords

Bax; Cytochrome C; Jing‐Si; inflammation; mitochondria; rheumatoid arthritis.

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