Department of Toxicology, School of Public Health, Shanxi Medical University, 56 Xin-Jian South Road, Taiyuan, 030001, Shanxi, China.
Department of Cardiology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Biol Trace Elem Res. 2023 Jul;201(7):3290-3299. doi: 10.1007/s12011-022-03426-w. Epub 2022 Sep 27.
Arsenic is a toxic metal, which ultimately leads to cell apoptosis. TLR4 signaling pathway played a key role in immunomodulatory. Therefore, alterations in related proteins on the TLR4 signaling pathway induced by arsenic exposure was systematically reviewed and analyzed by meta-analysis. Some databases were searched including PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and WANFANG MED ONLINE. The results of NF-κB, IKK, NF-κBp65, phospho-NF-κBp65, and TLR4 expressions were analyzed by Review Manage 5.3. In the arsenic intervention group, NF-κB, phospho-NF-κBp65, and TLR4 expression levels were higher than the control group, respectively. SMD and 95%CI were 11.29 (6.34, 16.24), 4.71(1.73, 7.68), and 5.79 (-4.22, 15.80). Compared to controls, in the exposed group, IKK levels were found to be 38.11-fold higher (Z = 0.97; P = 0.33); NF-κBp65 levels were found to be 0.92-fold higher (Z = 3.33; P = 0.0009) for normal cells and tissue, while IKK levels were found to be 5.18-fold lower (Z = 5.34; P < 0.0001); NF-κBp65 levels were found to be 2.01-fold lower (Z = 3.87; P = 0.0001) for abnormal cells. With comparing of low dose, high dose of arsenic exposure was found to reduce the expression of NF-κB, but increase the expression of NF-κBp65. This review supports the alterations in related proteins on the TLR4 signaling pathway induced by arsenic exposure, which is helpful to provide theoretical basis for the mechanism of toxicity of arsenic-induced immune system damage.
砷是一种有毒金属，最终导致细胞凋亡。TLR4 信号通路在免疫调节中起着关键作用。因此，通过荟萃分析系统地综述和分析了砷暴露引起的 TLR4 信号通路相关蛋白的改变。检索了一些数据库，包括 PubMed、Web of Science、中国知网（CNKI）和万方医学在线。使用 Review Manage 5.3 分析 NF-κB、IKK、NF-κBp65、磷酸化 NF-κBp65 和 TLR4 的表达。在砷干预组中，NF-κB、磷酸化 NF-κBp65 和 TLR4 的表达水平均高于对照组。SMD 和 95%CI 分别为 11.29（6.34，16.24）、4.71（1.73，7.68）和 5.79（-4.22，15.80）。与对照组相比，暴露组 IKK 水平高 38.11 倍（Z=0.97；P=0.33）；正常细胞和组织中 NF-κBp65 水平高 0.92 倍（Z=3.33；P=0.0009），而 IKK 水平低 5.18 倍（Z=5.34；P<0.0001）；NF-κBp65 水平低 2.01 倍（Z=3.87；P=0.0001）在异常细胞中。与低剂量相比，高剂量砷暴露降低了 NF-κB 的表达，但增加了 NF-κBp65 的表达。本综述支持砷暴露引起的 TLR4 信号通路相关蛋白的改变，这有助于为砷诱导的免疫系统损伤的毒性机制提供理论依据。
Zotero 插件