Relationship between p38 signaling pathway and arsenic-induced apoptosis: a meta-analysis

Arsenic exposure could induce apoptosis and cause related cancer. It was reported that p38 signaling pathway played a key transcriptional regulatory factor in arsenic-induced apoptosis. However, there were certain disputable questions about this point of opinion. Therefore, the relationship between p38 signaling pathway and arsenic-induced apoptosis was systematically reviewed and analyzed by meta-analysis. Twelve essays were analyzed with StataSE15.0 and Review Manager 5.3. The regulatory variables, such as normal cells and cancer cells, arsenic exposure time and exposure dose were analyzed by the subgroup analysis. The comprehensive effects were compared and analyzed by SMD method. Publication bias, the monolithic impact and heterogeneity were inspected. Subgroup analysis showed, when arsenic exposure was >= 5 mu mol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated. When arsenic exposure was < 5 mu mol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated. Arsenic exposure time (>= 48 h) or arsenic exposure dose (>= 5 mu mol/l or < 5 mu mol/l) can promote the expression of p38. Arsenic exposure time was >= 48 h or exposure dose was < 5 mu mol/l in cancer cells, arsenic exposure dose was >= 5 mu mol/l or exposure time was < 48 h in normal cells, and they are statistically significant in the expression of p38. This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.