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目的 :研究血管紧张素Ⅱ (AngⅡ )对小鼠腹腔巨噬细胞 (MPM )胰岛素样生长因子 1受体 (IGF 1R)、磷酸化的细胞外信号调节激酶 (p ERK)、Bcl 2和Bax蛋白表达水平的影响 ,探讨AngⅡ影响MPM存活的机制。方法 :利用免疫细胞化学的方法 ,检测IGF 1R、p ERK、Bcl 2和Bax蛋白的表达。 结果 :AngⅡ可明显增加IGF 1R的表达 ,呈浓度和时间依赖性 (P <0 .0 1)。AngⅡ可明显增加 p EKR(P <0 .0 1) ,呈浓度依赖性 ;刺激5min时 ,p ERK表达最高。预先给予α IR 3或PD980 5 9,p ERK的表达明显降低 ,呈浓度依赖性 (P <0 .0 1)。AngⅡ可刺激ERK转核 ,给予α IR 3或PD980 5 9后 ,转核现象消失。AngⅡ明显增加Bcl 2的表达 (P <0 .0 1) ,而降低Bax的表达 (P <0 .0 1) ,呈浓度和时间依赖性 ;预先给予α IR 3或PD980 5 9,Bcl 2的表达明显降低 (P <0 .0 1) ,Bax表达明显增高 (P <0 .0 1) ,呈浓度依赖性。结论 :AngⅡ增加MPMIGF 1R蛋白的表达 ,后者激动下游介导子ERK ,ERK磷酸化增加凋亡抑制基因Bcl 2蛋白的表达 ,降低促凋亡基因Bax蛋白的表达 ,从而促进MPM存活 ,并且可能有多种途径参与介导AngⅡ诱导MPM存活
AIM: To investigate the effects of Ang Ⅱ on the expression of insulin-like growth factor 1 receptor (IGF 1R), phosphorylated extracellular signal-regulated kinase (p ERK), Bcl 2 and Bax protein in mouse peritoneal macrophages (MPM) Expression of the impact of Ang Ⅱ to explore the mechanism of MPM survival. Methods: Immunocytochemistry was used to detect the expression of IGF 1R, p ERK, Bcl 2 and Bax. Results: Ang Ⅱ significantly increased IGF 1R expression in a concentration- and time-dependent manner (P <0.01). Ang Ⅱ significantly increased p EKR (P <0.01) in a concentration-dependent manner; p ERK expression was highest at 5 min stimulation. The expression of p ERK was significantly reduced in a concentration-dependent manner (P <0.01) when α IR 3 or PD980 5 9 was given in advance. AngⅡ stimulated the nuclear translocation of ERK, and the nuclear translocation disappeared after α IR 3 or PD980 5 9 administration. Ang Ⅱ significantly increased the expression of Bcl 2 (P <0.01) and decreased the expression of Bax (P <0.01) in a dose- and time-dependent manner. AngⅡ was pretreated with α IR 3 or PD980 5 9, and Bcl 2 (P <0.01), and the expression of Bax was significantly increased (P <0.01) in a concentration-dependent manner. CONCLUSION: AngⅡ increases the expression of MPMIGF-1R, which activates downstream ERK and ERK phosphorylation to increase the expression of apoptosis-inhibiting gene Bcl-2 and decrease the expression of Bax protein, thereby promoting the survival of MPM A variety of pathways are involved in mediating Ang II-induced MPM survival