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一种新的红细胞降压因子抗血管老化及其作用机制

Mechanism of a new erythrocyte-derived depressing factor for anti-vascular aging

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【作者】 王玉堂文允镒石磊庞焕马宁符莹莹

【Author】 Wang Yu-tang, Wen Yun-yi , Shi Lei, Pang Huan, Ma Ning, Fu Ying-ying ( Department of Physiology, Institute of Basic Medical Sciences , CAMS, School of Basic Medicine , PUMC. Beijing 100005)

【机构】 中国医学科学院基础医学研究所-中国协和医科大学基础医学院生理室中国医学科学院基础医学研究所-中国协和医科大学基础医学院生理室 北京 100005北京 100005北京 100005

【摘要】 目的 观察红细胞源性降压因子(EDDF)对钙超载(CaO)大鼠血管的保护作用。方法 选用CaO大鼠和正常大鼠,用离体动脉环灌流法观察EDDF对CaO大鼠胸主动脉、肠系膜二级阻力血管的舒张作用;用透射电镜观察EDDF对CaO大鼠主动脉血管平滑肌细胞(VSMC)超微结构的影响;分别用黄嘌呤氧化法和DTNB比色法观察EDDF对CaO大鼠血管组织中超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的影响;用无机磷方法测定ED—DF对CaO大鼠血管组织中Ca2+-ATPase的影响。结果 EDDF可以明显舒张CaO大鼠胸主动脉及肠系膜二级阻力血管(P<0.05或P<0.01),可以明显改善VSMC超微结构的异常,可以增加血管组织中SOD、GSH的活性(P<0.05),可以改善血管组织中Ca2+-ATPase活性的异常(P<0.05)。结论 EDDF可以通过舒张血管平滑肌,降低血管的异常反应性,调节钙离子代谢,增加血管抗氧化的能力,改善VSMC超微结构异常,而起到抗血管老化的作用。

【Abstract】 OBJECTIVE To investigate the vascular protective effect of a novel erythrocyte-derived depressing factor (EDDF) on calcium overload rats. METHODS The isolated thoracic aorta and mesentery vessel rings were used to examine the vasodilation effect of EDDF. The activities of superoxide dismutase (SOD) and glotathione-SH (GSH) in aorta were determined with xanthine oxidimetry and dithio-bis (2-nitrobenzoic acid) (DTNB) chromatome-try. The activity of Ca2+ -ATPase in vascular tissue was assessed by inorganic phosphate assay. The ultrastructure of vascular smooth muscle cells (VSMCs) was observed with transmission electron microscope. RESULTS EDDF (10-3g · mL-1) could significantly relax thoracic aorta and mesentery resistance vessels (P<0. 05) and significantly increase the activities of SOD, GSH and Ca2+-ATPase in vascular tissue (P<0. 05). EDDF also improved the ultra-structural lesion of VSMCs in calcium overload rats. CONCLUSIONS EDDF has protective effects on the blood vessels of calcium overload rats via multi-pathways, including decreasing the vascular response to vasoconstrictor, increasing the vascular ability against oxidative reaction, modulating Ca2+metabolism, and improving the ultrastructural lesion of VSMCs.

【基金】 国家自然科学基金项目(30240064,30070281)
  • 【文献出处】 中南药学 ,Central South Pharmacy , 编辑部邮箱 ,2003年02期
  • 【分类号】R96
  • 【被引频次】1
  • 【下载频次】81
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