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作 者:秦旭平[1] 任俊芳[1] 田海宏[1] 谌赟[1] 陈临溪[1]
机构地区:[1]南华大学药物药理研究所,湖南衡阳421001
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)
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.
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