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缺血预处理改善心肌钙超载后胰岛素抵抗 被引量:1

Ischemic preconditioning improves myocardial insulin resistance after calcium overload in rat cardiac myocytes
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摘要 目的步探讨缺血预处理对心肌细胞钙超载后胰岛素敏感性的影响。方法采用Langendorff灌流装置逆行主动脉插管灌注,胶原酶消化法分离获取成年大鼠心肌细胞。将心肌细胞分5个组:正常对照组,实验组1(ionomycin0.5μmol/L),实验组2(ionomycin0.5μmol/L+IP),实验组3(ionomycin1.0μmol/L),实验组4(ionomycin1.0μmol/L+IP),应用同位素示踪技术观察胰岛素刺激大鼠心肌细胞的葡萄糖摄取效应,评价心肌细胞的胰岛素敏感性。结果各组心肌细胞活性比率无明显降低(P>0.05)。对照组心肌细胞静息[Ca2+]i为(117.80±22.41)nmol/L,实验1,2组心肌细胞经过(ionomycin0.5μmol/L)处理1h后,[Ca2+]i明显高于对照组,但两组间无统计学差异(260.49±33.06)nmol/L,(278.03±23.46)nmol/Lvs(117.80±22.41)nmol/L;实验3,4组心肌细胞经过(ionomycin1.0μmol/L)处理1h后,实验3,4组心肌细胞[Ca2+]i明显高于实验1,2组和对照组,但两组间无统计学差异(391.91±20.01)nmol/L,(379.91±23.92)nmol/Lvs(260.49±33.06)nmol/L,(278.03±23.46)nmol/Lvs(117.80±22.41)nmol/L,(P<0.05)。胰岛素(20IU/L)能促进各组心肌细胞的葡萄糖摄取,分别为(56.86±6.89)μmol/105cells/10min,(31.10±7.62)μmol/105cells/10min,(40.12±6.90)μmol/105cells/10min,(22.26±5.92)μmol/105cells/10min,(32.33±6.06)μmol/105cells/10min。胰岛素刺激各实验组心肌细胞葡萄糖摄取较对照组心肌细胞葡萄糖摄取降低(P<0.05),胰岛素刺激实验组2,4心肌细胞的葡萄糖摄取虽较对照组降低,但是与无缺血预处理相比葡萄糖摄取有所增加(P<0.05)。结论缺血预处理对ionomycin导致的心肌细胞的钙超载没有影响,但是能改善钙超载心肌细胞的胰岛素抵抗。 Objective To investigate the effect of ischemic preconditioning (IP) on insulin sensitivity after cardiomyocyte calcium overload.Methods Adult rat cardiac myocytes were obtained through Langendorff perfusion with retrograde aortic infusion and collagenase digestion.Myocardial cells were divided into 5 groups,normal control group,experimental group 1 (ionomycin 0.5 μmol/L),experimental group 2 (ionomycin 0.5 μmol/L+IP),experimental group 3 (ionomycin 1.0 μmol/L),the experimental group 4 (ionomycin 1.0 μmol/L+IP).The glucose uptake of cardiomyoctyes stimulated by insulin was detected with isotopic tracer technique.Results Rate of cardiac cell activity in each group had no significant decrease (P〈0.05).Resting [Ca2+]i in normal cardiac muscle cells was (117±22.41) nmol/L,while for the cells of experimental groups 1 and 2,it was significantly higher than normal cells,but there was no significant difference between them after 1 hour’s treatment of 0.5 μmol/L ionomycin [(260.00±33.06) and (278±23.46) nmol/L respectively].The [Ca^2+]i in experimental groups 3 and 4 was (391.00±20.01),and (379.00±23.92) nmol/L respectively,which were significantly higher than those of experimental groups 1 and 2,and control group (P〈0.05).But there was no obvious difference between them.Insulin of 20 IU/L promoted glucose uptaking in the myocardial cells in each group,which were (56.86±6.89),(31.10±7.62),(40.12±6.90),(22.26±5.92),and (32.33±6.06) μmol/(105cells·10 min) respectively in control,and experimental groups 1,2,3 and 4.There were significantly lesser glucose uptake in the insulin-stimulated myocardial cells from all experimental groups than in the cells of the control group (P〈0.05).Insulin-stimulated myocardial cells in experimental groups 2 and 4 though had lower glucose uptake than the control group,but their glucose uptake were higher in comparison with non-ischemic preconditioning group (P〈0.05).Conclusion IP has no effect on ionomycin-induced calcium overload in myocardial cells,but can improve myocardial insulin resistance after calcium overload.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2010年第10期1068-1070,共3页 Journal of Third Military Medical University
关键词 心肌细胞 胰岛素抵抗 缺血预处理 cardiomyocyte insulin resistance ischemic preconditioning
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