Rehime Yapar, Özgül Soysal Gündüz, Feyzan Özdal Kurt, Mehmet Korkmaz
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Consent forms were obtained from all individuals participating the study, blood samples were taken, and peripheral blood mononuclear cells were isolated. Isolated cells were exposed to low-dose and high-dose boric acid and calcium fructoborate in cell culture. Treg and Th17 cell populations were analyzed by flow cytometry after 48 h of exposure. IL-2, IL-6, IL-17, IL-23, TNF-α, and TGF-β levels in the culture medium were tested by ELISA method. At the end of the study, in healthy controls, high-dose BA improved the Treg/Th17 population but could not display similar effects on RA and SLE group. However, both boric acid and calcium fructoborate at different doses showed an increasing effect on Ror-γt in RA and SLE group. Different doses of BA and CaF treatment found to have a variable effect on cytokine. Both BA and CaF in low doses decreased TNF-α levels in RA group which shows that these boron compounds could contribute positively to the treatment of autoimmune diseases.</p>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Effect of Boric Acid and Calcium Fructoborate on T Helper Cell Differentiation by Influencing Foxp3 and Ror-γt in Rheumatoid Arthritis and Systemic Lupus Erythematosus.\",\"authors\":\"Rehime Yapar, Özgül Soysal Gündüz, Feyzan Özdal Kurt, Mehmet Korkmaz\",\"doi\":\"10.1007/s12011-024-04425-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Many animal and human studies indicate that boric acid and calcium fructoborate have effects on helper T cells in immunity. 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引用次数: 0
摘要
许多动物和人体研究表明,硼酸和果硼酸钙对免疫系统中的辅助性 T 细胞有影响。我们的研究旨在评估硼酸和果酸钙对类风湿性关节炎和系统性红斑狼疮患者外周血样本中分离的单核细胞中 Treg(CD4+Foxp3+)和 Th17(CD4+Ror-γt+)细胞群及相关细胞因子水平的影响。新确诊的类风湿性关节炎患者(10 人)、系统性红斑狼疮患者(5 人)和健康人(9 人)都参与了这项研究。研究人员获得了所有参与研究人员的同意书,采集了血液样本,并分离了外周血单核细胞。分离出的细胞在细胞培养过程中暴露于低剂量和高剂量的硼酸和果硼酸钙。暴露48小时后,用流式细胞术分析Treg和Th17细胞群。培养液中的 IL-2、IL-6、IL-17、IL-23、TNF-α 和 TGF-β 水平用 ELISA 方法进行检测。研究结束时,在健康对照组中,高剂量 BA 可改善 Treg/Th17 群体,但对 RA 和系统性红斑狼疮组没有类似作用。然而,不同剂量的硼酸和果硼酸钙对 RA 组和系统性红斑狼疮组的 Ror-γt 均有增加作用。不同剂量的硼酸和果酸钙对细胞因子的影响不尽相同。低剂量的硼酸和钙硼酸盐都能降低RA组的TNF-α水平,这表明这些硼化合物能对自身免疫性疾病的治疗起到积极作用。
The Effect of Boric Acid and Calcium Fructoborate on T Helper Cell Differentiation by Influencing Foxp3 and Ror-γt in Rheumatoid Arthritis and Systemic Lupus Erythematosus.
Many animal and human studies indicate that boric acid and calcium fructoborate have effects on helper T cells in immunity. The aim of our study is to evaluate the effects of boric acid and calcium fructoborate on Treg (CD4+Foxp3+) and Th17 (CD4+Ror-γt+) cell populations and related cytokine levels in mononuclear cells isolated from peripheral blood samples of rheumatoid arthritis and systemic lupus erythematosus patients. Newly diagnosed rheumatoid arthritis (n = 10) patients, systemic lupus erythematosus (n = 5) patients, and healthy individuals (n = 9) were included in this study. Consent forms were obtained from all individuals participating the study, blood samples were taken, and peripheral blood mononuclear cells were isolated. Isolated cells were exposed to low-dose and high-dose boric acid and calcium fructoborate in cell culture. Treg and Th17 cell populations were analyzed by flow cytometry after 48 h of exposure. IL-2, IL-6, IL-17, IL-23, TNF-α, and TGF-β levels in the culture medium were tested by ELISA method. At the end of the study, in healthy controls, high-dose BA improved the Treg/Th17 population but could not display similar effects on RA and SLE group. However, both boric acid and calcium fructoborate at different doses showed an increasing effect on Ror-γt in RA and SLE group. Different doses of BA and CaF treatment found to have a variable effect on cytokine. Both BA and CaF in low doses decreased TNF-α levels in RA group which shows that these boron compounds could contribute positively to the treatment of autoimmune diseases.