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胰升糖素样肽1对乳鼠心肌细胞缺氧／复氧损伤的保护机制

The mechanism of the effect of glucagon-like peptide-1 on injury to neonatal rat cardiomyocytes induced by hypoxia-reoxygenation
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摘要 观察胰升糖素样肽1（glucagon—likepeptide-1，GLP-1）对原代培养的心肌细胞在缺氧／复氧条件下损伤的影响及机制。结果显示，缺氧／复氧使乳酸脱氢酶活性[（210．0±11，5）对（101．4±6．5）U／L]、细胞凋亡率[（8．138±1．512）对（0．575±0．168）％]和半胱氨酸天冬氨酸蛋白酶3活性[（44．52±5．69）对（19．98±1．97），均P〈0．01]均升高，GLP-1能直接作用心肌细胞，并对其在缺氧／复氧的损伤具有抑制作用[乳酸脱氢酶活性（190．2±9．0）U／L，细胞凋，亡率（2．688±0．580）％，半胱氨酸天冬氨酸蛋白酶3活性30．34±4．18]，该作用可能与磷脂酰肌醇3激酶（P13K）／Akt介导的抗细胞凋亡作用有关。 To study the possible mechanism ol the ettect of gtucagon-hke peptlde-1 （ GLF-1） on injury to neonatal rat cardiomyocytes induced by hypoxia-reoxygenation. Lactate dehydrogenase activity [ （210. 0± 11.5 ）vs （101.4±6.5） U/L] ,apoptosis rate [ （8. 138±1. 512）vs（0,575±0. 168）% ] ,and caspase-3 activity [ （44.52±5.69 ）vs （ 19.98 ± 1.97 ） , all P〈0.01 ] were all increased after hypoxia-reoxygenation. GLP-1 appears to directly act on cardiomyocytes and to protect them from hypoxia-reoxygenation injury [ lactate dehydrogenase （190.2±9.0）U/ L, apoptosis rate （2. 688±0. 580） % , caspase-3 activity 30.34 ±4. 18 ] mainly by inhibiting the apoptosis probably via the PI3K/Akt signaling pathways.
作者 谢云 沙伟伟 周雪 王绍欣 汪玮琳 韩丽萍 王家驰 于德民
机构地区 天津医科大学代谢病医院糖尿病神经内科 北京市昌平区医院 保定市中国人民解放军第
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 2010年第2期146-147,共2页 Chinese Journal of Endocrinology and Metabolism
关键词 胰升糖素样肽1 缺氧/复氧 细胞凋亡 半胱氨酸天冬氨酸蛋白酶3 Glucagon-like peptide-1 Hypoxia-reoxygenation Apoptosis Caspase-3
分类号 R587.1 [医药卫生—内分泌]
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参考文献12

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中华内分泌代谢杂志
2010年 第2期

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