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杨丽儒, 杨育红, 梁灵君, 孙雪芳, 李洪秀, 王洪新. 腺苷对脂多糖致大鼠心肌细胞肥大影响[J]. 中国公共卫生, 2013, 29(10): 1460-1462. DOI: 10.11847/zgggws2013-29-10-18
引用本文: 杨丽儒, 杨育红, 梁灵君, 孙雪芳, 李洪秀, 王洪新. 腺苷对脂多糖致大鼠心肌细胞肥大影响[J]. 中国公共卫生, 2013, 29(10): 1460-1462. DOI: 10.11847/zgggws2013-29-10-18
YANG Li-ru, YANG Yu-hong, LIANG Ling-jun.et al, . Effects of adenosine on lipopolysaccharide induced myocardial cell hypertrophy in neonatal rats[J]. Chinese Journal of Public Health, 2013, 29(10): 1460-1462. DOI: 10.11847/zgggws2013-29-10-18
Citation: YANG Li-ru, YANG Yu-hong, LIANG Ling-jun.et al, . Effects of adenosine on lipopolysaccharide induced myocardial cell hypertrophy in neonatal rats[J]. Chinese Journal of Public Health, 2013, 29(10): 1460-1462. DOI: 10.11847/zgggws2013-29-10-18

腺苷对脂多糖致大鼠心肌细胞肥大影响

Effects of adenosine on lipopolysaccharide induced myocardial cell hypertrophy in neonatal rats

  • 摘要: 目的探讨腺苷对脂多糖诱导乳鼠心肌细胞肥大的影响及作用机制。方法原代培养新生大鼠心肌细胞,以脂多糖1 mg/L诱导心肌细胞肥大,观察不同浓度腺苷对肥大心肌细胞影响,以计算机图像分析系统检测细胞体积,逆转录聚合酶链式反应法检测心房钠尿肽(ANP)mRNA,western blot法检测心肌细胞Toll样受体4(TLR4)的蛋白量,酶联免疫吸附试验检测肿瘤坏死因子(TNF-α)的含量。结果腺苷能有效抑制脂多糖诱导的心肌肥大,与模型组比较,低、中、高剂量腺苷组细胞体积分别减小15.6%、27.1%和32.8%(P<0.05),心肌细胞的ANP mRNA表达均较模型组降低(P<0.01);与脂多糖组比较,0.25、1、4 mg/L腺苷组TLR4蛋白表达(0.56±0.04)、(0.47±0.02)均降低(P<0.05),细胞外液TNF-α含量(30.8±4.1)、(22.7±2.9)、(19.1±3.7) pg/mL均减少(P<0.01)。结论腺苷对脂多糖诱导的乳鼠心肌细胞有保护作用,其机制可能与抑制TLR4表达有关。

     

    Abstract: Objective To investigate the effects and mechanism of adenosine(ADO)on lipopolysaccharide(LPS)-induced neonatal rat cardiomyocyte hypertrophy.Methods The hypertrophy of primary cardiac cells of neonatal rat was induced by 1 mg/L LPS and the effect of different concentrations of adenosine on cardiac hypertrophy was observed.The size of cardiomyocytes was measured wtih a computer photograph analysis system and the expression of atrial natriuretic peptide mRNA was determined by reverse transcription PCR.Toll like receptor 4(TLR4)and tumor necrosis factor-α(TNF-α)were determined with western blot and enzyme-linked immunosorbent assay.Results Adenosine inhibited lipopolysaccharide-induced cardiac hypertrophy,with the decreased volume of 15.6%,27.1%,and 32.8% for low,moderate,and high ADO treament compared with that of model group(P<0.05 for all).The expression of atrial natriuretic peptide mRNA also decreased(P<0.01).ADO treatment abolished the inflammatory response induced by LPS,which was partially via attenuating TLR 4 signal pathway(P<0.05).The TNF-α decreased obviously by 56.3%,67.8%,and 72.9% at ADO doses of 0.25,1.00,and 4.00 mg/L(P<0.01 for all).ConclusionAdenosine has a protective effect on LPS-induced cardiac hypertrophy.The mechanism may be related to the inhibition of TLR 4.

     

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