Protective Effect of Apigenin on Acrylonitrile-Induced Inflammation and Apoptosis in Testicular Cells via the NF-κB Pathway in Rats.

Apigenin (AP) as a plant flavonoid is found to attenuate acrylonitrile (ACN) toxicity by reducing ROS production and inhibiting apoptosis. Therefore, the present study aimed to evaluate the role of AP on ACN-induced inflammation and apoptosis in germ cells and whether it is through the NF-κB signaling pathway. AP increased the concentrations of lactate dehydrogenase isozyme (LDH) and sorbitol dehydrogenase (SDH), while the concentrations of interleukin β (IL-1β), tumor-necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were significantly reduced. AP could downregulate the expression of the nuclear factor of kappa B (NF-κB) and inhibit phosphorylation of the inhibitory κBα (IκBα). Cleaved caspase-3 was also upregulated by AP, and the apoptotic were less than those in the ACN group. These results suggest that AP might improve maturation and energy metabolism of testes, inhibit NF-κB activation. Then AP could further downregulate NF-κB signal and inhibit the germ cell apoptosis and reduce inflammatory caused by ACN.