期刊文献+

二甲双胍对高糖状态下心肌细胞保护作用的研究

Study on Protective Effect of Metformin on Cardiomyocytes in High Glucose Medium
下载PDF
导出
摘要 【目的】探讨二甲双胍对高糖状态下心肌细胞发挥保护作用的机制。【方法】取原代培养24h的心肌细胞,分为6组(均n=15):对照组(不加任何处理)、高糖组(25mmol/L)、高渗组(甘露醇液)、二甲双胍组(25mmol/L高糖分别加入10mol/L5×10。mol/L、10。mol/L浓度的二甲双胍)。【结果】与对照组比较,高糖组白介素-1B(IL-1p)、白介素-6(IL-6)、B型利钠肽(BNP)、氨基末端脑钠肽前体(NT—proBNP)及casp—sae-3的表达水平明显升高(均P〈0.05);与高糖组比较,二甲双胍组IL-1p、IL-6、BNP、NT-proBNP及casp—sae-3的表达水平明显降低(均P〈0.05)。【结论】二甲双胍能够抑制炎症因子的表达,减轻高糖引起的心肌损伤。 [Objective]To explore the mechanism of protective effect of metformin on cardiomyocytes in high glucose medium. [Methods] Myocardial cells in primary culture for 24h were divided into control group( n = 15, without any treatment), high glucose group( n : 15, 25mmol/L), hypertonic group( n = 15, manni- tol solution) and metformin group( n = 15). The metformin group was given high glucose and supplemented with metformin 10-Smol/L, 5 X 10-5 mol/L and 10 4tool/L, respectively. [Results] Compared with control group, the expression of interleukin-1 beta (IL-113), interleukin-6 (IL-6), B-type natriuretic peptide (BNP), NT-proBNP and caspsae-3 in high glucose group obviously increased(all P (0.05). Compared with high glu- cose group, the expression of IL-1B, IL-6, BNP, NT-proBNP and caspsae-3 in metformin group obviously de- creased(all P (0.05). [Conclusion] Metformin can inhibit the expression of inflammatory factors and reduce hyperglycemia-induced cardiomyocyte injury.
作者 张婷 文重远
出处 《医学临床研究》 CAS 2013年第2期258-260,共3页 Journal of Clinical Research
关键词 肌细胞 心脏 二甲双胍 药理学 葡萄糖 myocytes, cardiac metformin/PD glucose
  • 相关文献

参考文献13

  • 1Boudina S, Abel ED. Diabetic cardiomyopathy revisited[J]. Circulation , 2007,115(25) : 3213-3223.
  • 2Hsueh W, Abel ED, Breslow JL, et al . Recipes for creating animal models of diabetic cardiovascular disease[J]. Cite Res ,2007,100(10) :1415-1427.
  • 3Cai L,Wang Y,Zhou G, et al . Attenuation by metallothionein of early cardiac cell death via suppression of mitochondrial ox idative stress results in a prevention of diabetic cardiomyopa- thy[J]. J AmCollCardiol , 2006, 48(8):1688-1697.
  • 4Rolo Ap and Palmeira CM. Diabetes and mitochondrial func tion: Role of hyperglycemia and oxidative stress[J]. Toxicol Appl Pharmacol , 2006, 212(2):167-178.
  • 5Jensen J, Ma LP , Fu ML ,Svaninger D, et al . In ammation increases NT-proBNP and the NT proBNP/BNP ratio [J]. Clin Res Cardiol , 2010.99(7):445-452.
  • 6Tanaka T. Kanda T, Takahashi T, et al . Interleukin-6 in duced reciprocal expression of SERCA and natriuretic pep- tides mRNA in cultured rat ventricular myocytes[J]. J Int Med Res ,2004,32(1): 57-61.
  • 7Ma KK. Ogawa T and de Bold AJ . Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by pro-inammatory cytokines and by con- ditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase[J]. J Mol Cell Cardiol ,2004. 36(4):505- 513.
  • 8Wang XF, Zhang JY, Li L, et al . Metformin improves cardi ac function in rats via activation of AMP-activated protein ki nase[J]. Clin Exp Pharmacol Physiol , 2011,38 (2), 94 -101.
  • 9Bonnefont-Rousselot D, Raji B,Walrand S, Gardes Albert S, et al . An intracellular modulation of free radical production could contribute to the beneficial effects of metformin towards oxidative stress[J]. Metabolism , 2003,52 (5): 586-589.
  • 10Kewalramani G, Puthanveetil P, Wang F, et al . AMP activa- ted protein kinase confers protection against TNF-a-induced cardiac cell death[J]. Cardiovasc Res , 2009, 84 (1) : 42-53.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部