Puerarin prevents cadmium-induced disorder of testicular lactic acid metabolism in rats by activating 5' AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signaling pathway.

Abstract

Cadmium (Cd) interferes with the function of the male reproductive system; however, the molecular mechanism is poorly understood. This study aimed to evaluate the effect of puerarin (PU) on Cd-induced testicular lactic acid metabolism disorder. Weaning male Sprague-Dawley rats were pre-fed for 7 days, weighed, and randomly divided into four groups: Control group, CdAc2 group, CdAc2 + PU group, PU group. The results showed that Cd accumulated in the testis, the testicles became congested and shrank, and the testis index decreased in the rats treated in the CdAc2 group. Cadmium exposure reduced the serum concentration of testosterone, and the concentration of lactic acid and pyruvate in the testis. Cd decreased testicular superoxide dismutase activity and total antioxidant capacity, and increased testicular malondialdehyde levels. Cd reduced the level of ATP, glycolytic gene expression, and lactate production-related proteins in the testis. Cd also decreased the expression of 5' AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) signaling pathway-related proteins in the testis. However, these negative effects were attenuated by PU administration. In summary, Cd reduces the production of lactic acid in the testis of rats, while PU administration restores the production of lactic acid and reduces the toxicity of Cd to the testis of rats.