首页> 外文期刊>Biological trace element research >Selenium Antagonizes the Lead-Induced Apoptosis of Chicken Splenic Lymphocytes In Vitro by Activating the PI3K/Akt Pathway
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Selenium Antagonizes the Lead-Induced Apoptosis of Chicken Splenic Lymphocytes In Vitro by Activating the PI3K/Akt Pathway

机译:通过激活PI3K / AKT途径,硒拮抗体外培养的鸡脾淋巴细胞凋亡凋亡

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摘要

Lead (Pb) pollution has become one of the most serious global ecological problems. In animals, Pb ingestion induces apoptosis in many tissues. However, the mechanisms by which Pb induces apoptosis in chicken splenic lymphocytes in vitro via the PI3K/Akt pathway and the antagonistic effect of selenium (Se) on Pb remain unclear. Therefore, we established the in vitro Se-Pb interaction model in chicken splenic lymphocytes and examined the frequency of apoptotic cells using acridine orange/ethidium bromide (AO/EB) staining and the TdT-mediated dUTP nick end labeling assay and detected the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), as well as the levels of malondialdehyde (MDA) and reactive oxygen species (ROS). The expression of PI3K/Akt pathway-related genes was also examined by qRT-PCR and western blotting. MDA and ROS levels were markedly increased, whereas the activities of GPx, SOD, and CAT were significantly decreased; the levels of the PI3K, Akt, and Bcl-2 messenger RNAs (mRNAs) and proteins were decreased; and the levels of the p53, Bax, cytochrome c (Cyt-c), caspase 3, and caspase 9 mRNAs and proteins were increased in the Pb group. In addition, the frequency of apoptotic cells was also significantly increased by the Pb treatment. However, Se supplementation during Pb exposure observably attenuated Pb-induced apoptosis; increased the levels of the PI3K, Akt, and Bcl-2 mRNAs and proteins; and decrease the levels of the p53, Bax, Cyt-c, caspase 3, and caspase 9 mRNAs and proteins in the chicken spleen. In conclusion, Pb exposure causes oxidative stress, inhibits the PI3K/Akt pathway, and subsequently induces apoptosis in chicken splenic lymphocytes in vitro, and these effects are partially attenuated by Se supplementation. To the best of our knowledge, this study is the first to reveal the antagonistic effect of Se on Pb-induced apoptosis of chicken splenic lymphocytes in vitro via the activation of the PI3K/Akt pathway.
机译:铅(PB)污染已成为最严重的全球生态问题之一。在动物中,PB摄入诱导许多组织中的细胞凋亡。然而,PB通过PI3K / AKT途径在体外诱导鸡脾淋巴细胞细胞凋亡的机制以及硒(SE)对PB的拮抗作用仍不清楚。因此,我们在鸡脾淋巴细胞中建立了体外SE-PB相互作用模型,并使用吖啶橙/乙锭(AO / EB)染色和TDT介导的DUTP缺口末端标记测定检测和检测到凋亡细胞频率。谷胱甘肽过氧化物酶(GPX),超氧化物歧化酶(SOD)和过氧化氢酶(CAT),以及丙二醛(MDA)和反应性氧(ROS)的水平。通过QRT-PCR和Western印迹检查PI3K / AKT途径相关基因的表达。 MDA和ROS水平显着增加,而GPX,SOD和CAT的活动显着下降; PI3K,AKT和BCL-2信使RNA(MRNA)和蛋白质的水平降低;并且Pb组中P53,Bax,细胞色素C(Cyt-C),胱天蛋白3和Caspase 9 mRNA和蛋白质的水平增加。此外,通过PB治疗也显着增加凋亡细胞的频率。然而,在PB暴露期间SE补充可观察衰减的PB诱导的细胞凋亡;增加了PI3K,AKT和BCL-2 mRNA和蛋白质的水平;并降低P53,Bax,Cyt-C,Caspase 3和Caspase 9 mRNA和蛋白质中的水平。总之,Pb暴露导致氧化应激,抑制PI3K / AKT途径,随后在体外诱导鸡脾淋巴细胞中的细胞凋亡,并且这些效果通过补充部分衰减。据我们所知,本研究首先揭示SE对PB诱导的鸡脾淋巴细胞凋亡的拮抗作用,通过激活PI3K / AKT途径。

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