CAJ | 학술논문

观察胰升糖素样肽1(glucagon-like peptide-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(PBK)/Akt介导的抗细胞凋亡作用有关.
관찰이승당소양태1(glucagon-like peptide-1,GLP-1)대원대배양적심기세포재결양/복양조건하손상적영향급궤제.결과현시,결양/복양사유산탈경매활성[(210.0±11.5)대(101.4±6.5)U/L]、세포조망솔[(8.138±1.512)대(0.575±0.168)%]화반광안산천동안산단백매3활성[(44.52±5.69)대(19.98±1.97),균P<0.01]균승고,GLP-1능직접작용심기세포,병대기재결양/복양적손상구유억제작용[유산탈경매활성(190.2±9.0)U/L,세포조망솔(2.688±0.580)%,반광안산천동안산단백매3활성30.34±4.18],해작용가능여린지선기순3격매(PBK)/Akt개도적항세포조망작용유관.
To study the possible mechanism of the effect of glucagon-like peptide-1 (GLP-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 PBK/Akt signaling pathways.