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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
Environmental Toxicology ( IF 4.4 ) Pub Date : 2021-01-06 , DOI: 10.1002/tox.23096
Wenxuan Dong 1, 2, 3 , Kanglei Zhang 1, 2, 3 , Gang Liu 1, 2, 3 , Yun Tan 1, 2, 3 , Hui Zou 1, 2, 3 , Yan Yuan 1, 2, 3 , Jianhong Gu 1, 2, 3 , Ruilong Song 1, 2, 3 , Jiaqiao Zhu 1, 2, 3 , Zongping Liu 1, 2, 3
Affiliation  

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.

中文翻译:

葛根素通过激活 5' AMP 活化蛋白激酶 (AMPK)/sirtuin 1 (SIRT1) 信号通路预防镉诱导的大鼠睾丸乳酸代谢紊乱

镉 (Cd) 会干扰男性生殖系统的功能;然而,人们对其分子机制知之甚少。本研究旨在评估葛根素(PU)对镉诱导的睾丸乳酸代谢障碍的影响。断奶雄性Sprague-Dawley大鼠预饲7天,称重,随机分为4组:对照组、CdAc2组、CdAc2+PU组、PU组。结果显示CdAc2组大鼠睾丸内Cd蓄积,睾丸充血萎缩,睾丸指数下降。镉暴露降低了睾酮的血清浓度,以及睾丸中乳酸和丙酮酸的浓度。Cd 降低睾丸超氧化物歧化酶活性和总抗氧化能力,并增加睾丸丙二醛水平。Cd 降低了睾丸中 ATP 的水平、糖酵解基因的表达和与乳酸产生相关的蛋白质。Cd 还降低了睾丸中 5' AMP 活化蛋白激酶 (AMPK)/sirtuin 1 (SIRT1) 信号通路相关蛋白的表达。然而,这些负面影响通过 PU 给药减弱。综上所述,Cd减少了大鼠睾丸中乳酸的产生,而PU给药则恢复了乳酸的产生,降低了Cd对大鼠睾丸的毒性。
更新日期:2021-01-06
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