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

IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES
Shih-Wen Kao, Yu-Chun Chang, Feng-Huei Lin, Tai-Lung Huang, Tung-Sheng Chen, Shinn-Zong Lin, Kuan-Ho Lin, Wei-Wen Kuo, Tsung-Jung Ho, Chih-Yang Huang
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引用次数: 0

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.

靖西凉茶通过抑制HIG-82滑膜细胞中Bax和线粒体细胞色素C的释放来抑制H2O2诱发的炎症和细胞凋亡
炎症是人类抵御各种形式细胞损伤的内在保护机制;然而,不适当的炎症激活会导致组织损伤和细胞死亡。慢性炎症和氧化应激是类风湿性关节炎(RA)等自身免疫性炎症疾病的主要特征,目前尚未开发出有效的治疗方法。因此,在本研究中,我们研究了一种新型中草药制剂京四凉茶(JS)对 H2O2 诱导的 HIG-82 滑膜细胞炎症和细胞损伤的保护作用和分子机制。我们发现,在 2O2 诱导的病理性氧化应激(ROS)作用下,JS 并未对 HIG-82 细胞的存活率产生明显改变。有趣的是,JS 处理不仅降低了 ROS 水平,还以剂量依赖的方式显著抑制了胶原降解蛋白酶的蛋白表达。使用 JS 处理后,细胞的存活率提高,可以抵御 H2O2 诱导的毒性 ROS 水平。在炎症因子 H2O2、MIA、LPS 和 TNF-α 处理下,HIG-82 细胞中细胞保护因子 aggrecan、胶原蛋白 II 和 Bcl-2 的表达量增加,而 MMP-13、ADAMTS-2、细胞色素 C 和裂解 Caspase 3 的表达量则分别减少。有趣的是,JS处理的细胞保护作用归因于Bax线粒体定位的减少和H2O2处理的HIG-82细胞细胞质中细胞色素C释放的减少。总之,我们的研究结果表明,JS对RA的治疗具有一种新的保护机制,有可能作为一种辅助治疗或替代治疗方法用于缓解炎症性疾病。
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来源期刊
Environmental Toxicology
Environmental Toxicology 环境科学-毒理学
CiteScore
7.10
自引率
8.90%
发文量
261
审稿时长
4.5 months
期刊介绍: The journal publishes in the areas of toxicity and toxicology of environmental pollutants in air, dust, sediment, soil and water, and natural toxins in the environment.Of particular interest are: Toxic or biologically disruptive impacts of anthropogenic chemicals such as pharmaceuticals, industrial organics, agricultural chemicals, and by-products such as chlorinated compounds from water disinfection and waste incineration; Natural toxins and their impacts; Biotransformation and metabolism of toxigenic compounds, food chains for toxin accumulation or biodegradation; Assays of toxicity, endocrine disruption, mutagenicity, carcinogenicity, ecosystem impact and health hazard; Environmental and public health risk assessment, environmental guidelines, environmental policy for toxicants.
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