cAMP/PKA Signaling Pathway Induces Apoptosis by Inhibited NF-kappa B in Aluminum Chloride-Treated Lymphocytes In Vitro

文献类型: 外文期刊

第一作者: Xu, Feibo

作者: Xu, Feibo;Wang, Jing;Cao, Zheng;Song, Miao;Fu, Yang;Li, Yanfei;Zhu, Yanzhu

作者机构:

关键词: AlCl3;Lymphocytic apoptosis;cAMP/PKA signal pathway;NF-kappa B

期刊名称:BIOLOGICAL TRACE ELEMENT RESEARCH ( 影响因子:3.738; 五年影响因子:3.44 )

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收录情况: SCI

摘要: To explore the apoptosis mechanism in lymphocytes of rats induced by aluminum chloride (AlCl3) by activating cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway, the splenic lymphocytes of rats were cultured and exposed to different concentrations of AlCl3 for 24 h. The final concentrations of AlCl3 (AlCl3 center dot A 6H(2)O) in supernatant were 0 (control group, CG), 0.3 mmol/L (low-dose group, LG), 0.6 mmol/L (mid-dose group, MG), and 1.2 mmol/L (high-dose group, HG), respectively. Lymphocytes Apoptosis rate, intracellular cAMP content, PKA, survivin, B cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2-associated X protein (Bax) mRNA expressions, and the mRNA and protein expressions of nuclear factor-kappa-gene binding (NF-kappa B, p65) were detected, respectively. The results showed that apoptosis index of lymphocytes, cAMP content in intracellular and PKA mRNA expression were significantly upregulated, whereas NF-kappa B and survivin mRNA expressions, nuclear NF-kappa B (p65) protein expression, and the ratio of Bcl-2 and Bax mRNA expression were downregulated in the AlCl3-treated groups compared with those in CG. The results indicated that the activated cAMP/PKA signaling pathway induces apoptosis by inhibited NF-kappa B in AlCl3-treated lymphocytes in vitro.

分类号: Q5

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