摘要
目的探讨缺氧后复氧对肥大心肌细胞糖和脂肪酸的氧化效应。方法血管紧张素Ⅱ+去甲肾上腺素诱导原代培养大鼠心肌细胞肥大,采用[H3]-Leu掺入法和测定细胞表面积来鉴定心肌细胞肥大;通过体外培养心肌细胞的缺氧后复氧模拟缺血再灌注模型;采用同位素液闪计数法,测定细胞糖和脂肪酸的氧化及丙酮酸脱氢酶、肉碱脂酰转移酶活性。结果 0.1μmol/L血管紧张素Ⅱ+1μmol/L去甲肾上腺素使心肌细胞体积增大63.94%,[H3]-Leu掺入量增加181.54%(P<0.01),成功建立心肌细胞肥大模型。缺氧8 h,丙酮酸脱氢酶活性降低,糖氧化下降48%;复氧后,二者均上升到缺氧前的水平。缺氧8 h,肉碱脂酰转移酶活性降低,脂肪酸氧化下降约60%,复氧后,二者均逐渐上升到缺氧前的水平。结论缺氧时心肌细胞糖和脂肪酸氧化效应下降,复氧后二者逐渐恢复,丙酮酸脱氢酶和肉碱脂酰转移酶活性改变参与调节二者的变化。
Aim To explore effects of hypoxia-reoxygenation on glucose oxidation and fatty acid oxidation（FAO） of hypertrophied cardiomyocytes. Methods Cultured rat cardiomyocytes were induced to be hypertrophy by angiotention Ⅱ（AngⅡ） and norepinephrine（NE）,which was confirmed by -Leu incorporation in cardiomyocytes and detection surface area of cells.We established a model of post-hypoxia reoxygenation of cultured cardic cells in vitro.Glucose oxidation,FAO and acitivity of pyruvate dehydrogenase（PDH） and carnitine palmitoyltransferase（CPT） were determined by liquid scintillation counting. Results Surface area of cells increased by 63.94% and -Leu incorporation by 181.54%,when 0.1 μmol/L Ang Ⅱand 1 μmol/L NE were added in vitro.Activity of PDH decreased,and glucose oxidation decreased by 48%;Activity of PDH and glucose oxidation recovered to the level of prehypoxia at 8 hours of reoxygenation.Activity of CPT decreased,and FAO decreased by 60%;Activity of FAO and CPT recovered gradually to the level of prehypoxia during reoxygenation. Conclusion Glucose oxidation and fatty acid oxidation of hypertrophied cardiomyocyte decreased during hypoxia,and both recovered during reoxygenation.Activity of PDH and CPT was involved in these changes.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2010年第5期363-366,共4页
Chinese Journal of Arteriosclerosis
关键词
缺氧后复氧
肥大心肌细胞
能量代谢
Hypoxia-Reoxygenation
Hypertrophied Cardiomyocytes
Energy Metabolism
