Meta-analysis of TLR4 pathway-related protein alterations induced by arsenic exposure.

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.