摘要
目的探讨血红素氧合酶(HO)1在胰岛素对缺氧/复氧心肌细胞保护机制中的作用。方法体外培养SD乳鼠心肌细胞,分为7组常氧对照组,缺氧/复氧对照组,不同剂量胰岛素组(160、320、640、960mU/L),胰岛素加原卟啉锌组(胰岛素640mU/L、原卟啉锌10μmol/L)。除常氧对照组外,其余各组均给于缺氧3h,再复氧1h处理。检测心肌细胞HO1蛋白表达、HO活性、细胞生存率及乳酸脱氢酶(LDH)值。结果与缺氧/复氧对照组比较,各胰岛素组心肌细胞HO1蛋白表达显著增加,HO活性、细胞生存率显著增高,LDH显著降低。原卟啉锌能显著抑制HO活性,阻止胰岛素对心肌细胞的保护作用。结论胰岛素能够增加缺氧/复氧心肌细胞HO1的表达,增高HO活性,从而减轻心肌细胞缺氧/复氧损伤。
AIM: To explore the role of heme oxygense-1(HO-1) in the myocardial protection of insulin. METHODS: Neonatal cardiomyocytes of SD rats cultured in vitro, and then the study was performed according to different groups: Normoxia; Hypoxia-reoxygenation; Insulin(160, 320, 640, 960 mU/L); Insulin(640 mU/L) and Zinc Protoporphyrin IX (znpp,10 μmol/L). Except Normoxia, the other groups were subjected to 3 hours of hypoxia and 1 hour of reoxygenation. Expression of HO-1,HO activity, cell viability and lactate dehydrogenase (LDH) were detected. RESULTS: In comparison with control group, HO-1 expression, HO activity and cell viability increase, however, LDH levels decreases in insulin groups. Znpp could inhibit HO activity and blockade the myocardial protective mechanism of insulin. CONCLUSION: Insulin could reduce the hypoxia-reoxygenation injury of cardiomyocytes by increasing HO-1 expression and HO activity.
出处
《心脏杂志》
CAS
2005年第2期111-114,共4页
Chinese Heart Journal