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机构地区:[1]衡阳医学院心血管病研究所
出 处:《中国动脉硬化杂志》1995年第3期224-228,共5页Chinese Journal of Arteriosclerosis
摘 要:我室曾用C_(57)BL/6J品系小鼠腹膜巨噬细胞与10mg·L ̄(-1)氧化低密度脂蛋白孵育4天,建立了出现在早期动脉粥样硬化损伤中的巨噬细胞源性泡沫细胞的病理细胞模型,本文报道应用Ca ̄(2+)荧光指示剂技术及NADH氧化偶联差光谱变化的分析方法,检测了前述培养的泡沫样细胞的胞浆Ca ̄(2+)水平及膜上Ca ̄(2+)依赖性ATP酶活性。发现泡沫样细胞内的Ca ̄(2+)水平为对照组细胞的2.7倍,膜上Ca ̄(2+)依赖性ATP酶活性为后者的24%。实验结果提示,在巨噬细胞源性泡沫细胞的形成过程中,伴随着缓慢的Ca ̄(2+)内流或释放,这可能与膜上Ca ̄(2+)通道的持续开放及后期Ca ̄(2+)依赖性ATP酶的钝化有关。Previous study proved that it generated an in vitro model of macrophage-derived foam cell, namely, the characteristic pathological cell in the early atherosclerotic lesion to incubate C_(57) BL/6J mouse peritoneal macrophages with 10 mg·L ̄(-1) oxidized low density lipoprotein for 4 days. With the Ca ̄(2+) fluorescent indicator technique and NADH-oxidizingcoupling-spectrum-analysis method, we determined the intracellular Ca ̄(2+)-ATPase of the above cultured foam-like cell. The results indicated that the [Ca ̄(2+)]i level was 2. 7 times higher than that of control group cells, and the activity of Ca ̄(2+)-ATPase was 24% of that of the later cells. This supported that macrophage-derived foam cell formation is connected with the slow Ca ̄(2+) entry or release, which possibly derived from long-lasting openings of membranous Ca ̄(2+) channels and the inactivating of Ca ̄(2+)-ATPase at the late stage.
分 类 号:R543.502[医药卫生—心血管疾病]
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