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作 者:孙银平[1] 邢东琦[2] 汪香婷[2] 胡少勇[2] 白桦[3] 吴立玲[2]
机构地区:[1]新乡医学院病理生理学教研室,河南453003 [2]北京大学基础医学院生理学与病理生理学系,北京100083 [3]邮电总医院心内科,北京100032
出 处:《中国应用生理学杂志》2005年第2期166-169,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金资助课题(39870356)
摘 要:目的:研究血管紧张素Ⅱ(AngⅡ)对血管平滑肌细胞血小板源生长因子(PDGF)受体表达的影响。方法:采用大鼠主动脉球囊内皮剥脱术制备主动脉再狭窄模型,观察形态学变化;放免法测定主动脉AngⅡ含量;免疫印迹法测定主动脉PDGFβ受体含量,并与假手术组相比较。培养大鼠主动脉血管平滑肌细胞(VSMC),AngⅡ刺激正常培养的与洛沙坦预处理过的VSMC6h,测定PDGFβ受体含量。结果:球囊内皮剥脱术后14d,主动脉中层VSMC大量增殖,内膜显著增厚,AngⅡ含量显著升高(P<0.05),PDGFβ受体表达显著增强(P<0.05)。AngⅡ诱导VSMCPDGFβ受体表达显著增强(P<0.01),AngⅡ受体拮抗剂洛沙坦完全抑制AngⅡ对PDGFβ受体上调的诱导作用。结论:AngⅡ可通过其Ⅰ型受体诱导血管平滑肌细胞PDGF受体上调,这可能是AngⅡ促VSMC发生增殖的一个重要机制。Aim: To study the effect of angiotensin Ⅱ(AngⅡ) on platelet-derived growth factor(PDGF) receptor expression in vascular smooth muscle cell(VSMC). Methods: Restenosis model was established by balloon injury in rat aorta. The morphologic change and level of AngⅡ were measured at 14th day after operation. The expression of PDGF-β receptor was detected by Western blot.The cultured VSMC pretreated with or without losartan were treated with AngⅡ. Results: Compared with sham group, the sections of injured aorta showed marked intimal thickening with large numbers of VSMCs proliferation throughout intima and media, the level of AngⅡ obviously increased by 78.8%(P<0.05), the expression of PDGF-β receptor significantly increased by 83.9%(P<0.05) (at) 14 th day after operation. The expression of PDGF-β receptor in cultured VSMC treated with AngⅡ was higher than that of control group(P<0.01). The effect of AngⅡ was inhibited remarkably by pretreatment with losartan. Conclusion: AngⅡ can stimulate PDGF receptor expression in VSMC, it may be an important mechanism of AngⅡ-induced VSMC proliferation.
关 键 词:再狭窄 血管紧张素-Ⅱ 血小板源生长因子受体 血管 平滑肌
分 类 号:R331[医药卫生—人体生理学] Q74[医药卫生—基础医学]
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