摘要
目的观察降钙素基因相关肽（CGRP）对血管紧张素Ⅱ（AngⅡ）诱导血管平滑肌细胞（VSMC）增殖过程中细胞脂代谢的影响，探索影响脂代谢的腺苷酸活化蛋白激酶（AMPK）信号蛋白在该作用中的变化。方法贴块法体外培养大鼠胸主动脉平滑肌细胞（VSMC），取第3-10代用于实验。分别用CGRP或／和AngⅡ处理细胞。细胞计数法观察CGRP对AngⅡ诱导大鼠VSMC增殖的影响；油红O染色检测细胞内脂质含量；Western blot检测细胞p-AMPK、p-ERK1／2的表达。结果CGRP预处理能减少AngⅡ诱导的大鼠VSMC数目（P〈0．05）和细胞内脂质聚集的作用，在此过程中伴随细胞内p-AMPK、p-ERK1／2表达下调（P〈0．05）；CGRP8—37（CGRP受体拮抗剂）能拮抗CGRP对AngⅡ促增殖和脂代谢作用（P〈0．05）；PD98059（ERK1／2抑制剂）能部分拮抗CGRP对p—AMPK的抑制作用（P〈0．05）。结论CGRP能显著降低AngⅡ诱导大鼠VSMC增殖过程中的脂质代谢，其细胞内信号通路可能涉及到p—ERK1／2和p—AMPK信号蛋白。
Objective To investigate the effect of calcitonin gene- related peptide （ CGRP ） on the proliteration and lipid metabolism in vascular smooth muscle cells induced by angiotensin Ⅱ （ Ang Ⅱ ）, and further explore whether AMP - activated protein kinase （ AMPK ） involved in the cellular signal pathway. Methods Vascular smooth muscle cells （VSMC） were prepared from thoracic aorta of male Spragne - Dawley rat by the explanted method. The 3 - 10 passages of cells were used for the present studies. The cells number was counting under the microscope. Cellular lipid metabolism was tested by oil red O for fat staining. Western blotting was used to observe the expressions of p - ERK1/2, p - AMPK in VSMC. Results Ang Ⅱ increased the numbers and lipid contents in the VSMC. Pretreatment of the cell with CGRP significanfly inhibited VSMC proliferation and the lipid contents （P 〈 0.05 ）. Meanwhile, CGRP down -regulated expressions of p - AMPK and p - ERK1/2 induced by Ang Ⅱ, which were partly abolished by CGRP8 - 37 or PD98059, respectively. Conclusion CGRP significantly decreased the hypermetabolism of lipid induced by Ang Ⅱ in the VSMC. The intracellular signal pathway involved the ERK1/2 and p - AMPK signal kinases.
出处
《南华大学学报（医学版）》
2009年第1期1-4,共4页
Journal of Nanhua University(Medical Edition)
基金
湖南省自然基金资助课题(No.05JJ30042)
