College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Key Laboratory of the Provincial Education, Harbin, People's Republic of China.
Environ Sci Pollut Res Int. 2017 Sep;24(25):20342-20353. doi: 10.1007/s11356-017-9422-6. Epub 2017 Jul 13.
Cadmium (Cd) is a toxic heavy metal that can induce apoptosis. Selenium (Se) is a necessary trace element and can antagonize the toxicity of many heavy metals, including Cd. PI3K/AKT/Bcl-2 is a key survival signaling pathway that regulates cellular defense system against oxidative injury as well as cell proliferation, survival, and apoptosis. The antagonistic effects of Se on Cd-induced toxicity have been reported. However, little is known about the effect of Se on Cd-induced apoptosis in chicken kidneys via the PI3K/AKT/Bcl-2 signaling pathway. In the present study, we fed chickens with Se, Cd, or both Se and Cd supplements, and after 90 days of treatment, we detected the related index. The results showed that the activity of inducible nitric oxide synthase (iNOS) and concentration of nitric oxide (NO) were increased; activities of the mitochondrial respiratory chain complexes (complexes I, II, and V) and ATPases (the Na-K-ATPase, the Mg-ATPase, and the Ca-ATPase) were decreased; expression of PI3K, AKT, and Bcl-2 were decreased; and expression of Bax, Bak, P53, Caspase-3, Caspase-9, and cytochrome c (Cyt c) were increased. Additionally, the results of the TUNEL assay showed that the number of apoptotic cells was increased in the Cd group. By contrast, there was a significant improvement of the correlation indicators and occurrence of apoptosis in the Se + Cd group compared to the Cd group. In conclusion, our results confirmed that Se had a positive effect on ameliorating Cd-induced apoptosis in chicken kidney tissue by activating the PI3K/AKT/Bcl-2 signaling pathway.
镉（Cd）是一种有毒的重金属，可以诱导细胞凋亡。硒（Se）是一种必需的微量元素，可以拮抗许多重金属的毒性，包括 Cd。PI3K/AKT/Bcl-2 是一个关键的生存信号通路，调节细胞对氧化损伤以及细胞增殖、存活和凋亡的防御系统。已经有报道称硒对 Cd 诱导的毒性具有拮抗作用。然而，关于硒通过 PI3K/AKT/Bcl-2 信号通路对鸡肾脏中 Cd 诱导的细胞凋亡的影响知之甚少。在本研究中，我们用 Se、Cd 或 Se 和 Cd 补充剂喂养鸡，治疗 90 天后，检测相关指标。结果表明，诱导型一氧化氮合酶（iNOS）的活性和一氧化氮（NO）的浓度增加；线粒体呼吸链复合物（复合物 I、II 和 V）和 ATP 酶（Na-K-ATP 酶、Mg-ATP 酶和 Ca-ATP 酶）的活性降低；PI3K、AKT 和 Bcl-2 的表达降低；Bax、Bak、P53、Caspase-3、Caspase-9 和细胞色素 c（Cyt c）的表达增加。此外，TUNEL 检测结果表明 Cd 组的凋亡细胞数量增加。相比之下，Se + Cd 组与 Cd 组相比，相关指标和凋亡的发生有显著改善。总之，我们的结果证实，硒通过激活 PI3K/AKT/Bcl-2 信号通路，对改善鸡肾组织中 Cd 诱导的细胞凋亡具有积极作用。
