健康大鼠血管衰老性重塑与血管衰老相关基因的关系  

Relationship Between Vascular Aging Related Remodeling and Senescence Associated Genes in Health Rats

作　　者：单海燕[1] 白小涓[1] 韩璐璐[1] 张伟光[1] 陈香美[2] 

机构地区：[1]中国医科大学附属第一医院老年心血管科,辽宁省沈阳市110001 [2]中国人民解放军总医院肾内科全军肾病中心暨重点实验室,北京市100853

出　　处：《中国动脉硬化杂志》2008年第10期809-812,共4页Chinese Journal of Arteriosclerosis

基　　金：国家973重点基础研究发展规划项目(G2007CB507405)

摘　　要：目的通过研究健康大鼠血管衰老性重塑形态学变化及衰老相关基因表达,探讨血管衰老性重塑可能的分子调控机制,为临床有效干预血管衰老提供分子靶点。方法观察主动脉组织形态及内皮细胞显微结构变化,应用Western blotting分析4、10、16月和24月龄大鼠血管重塑p16INK4a和p21cip1蛋白表达变化。结果随增龄,大鼠主动脉管壁增厚,纤维化程度增高,内皮细胞形态呈现衰老改变,p16INK4a和p21cip1蛋白表达呈时间依赖性上调。结论血管衰老性重塑的分子机制之一可能与上调细胞周期蛋白p16INK4a和p21cip1的表达有关。进一步阐明其调控机制可为延缓血管衰老,防治动脉粥样硬化提供理论依据。Aim To observe the morphological changes in vascular aging - related remodeling, and p16INK4a ,p21cipl gene expression associated with senescence in healthy rats during natural aging. Methods Aortic structure and microstructure changes of vascular endothelial cell in 4, 10, 16, 24 months old rats were observed respectively, and the expressions of p16INK4a ,p21cipl protein were determined by Western-Blotting in the same periods. Results With aging, aorta wall thickened, fibrosis degree increased, endothelial cells appeared flattened and enlarged. The protein expressions of p16INK4a,p21cipl were increased in vascular aging - related remedeling, which suggests that p16INK4a,p21cipl activity may play an important role in regulating vascular senescence lifespan in vitro. Conclusion Vascular aging has its specific structural alterations, one of its molecular mechanisms might be associated with increasing the expression level of p16INK4a ,p21ciplwith aging. Further elucidating its underlying mechanism may provide theoretical basis for prevention and treatment of atherosclerosis.

关 键 词：生理学 血管衰老 动脉硬化 细胞周期 基因调控 P16INK4A p21cipl 

分 类 号：Q4[生物学—生理学]