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作 者:杨丽儒[1,2] 杨育红[1] 梁灵君[1] 孙雪芳[1] 李洪秀 王洪新[1]
机构地区:[1]辽宁医学院药理教研室,辽宁锦州121001 [2]盘锦市中心医院
出 处:《中国公共卫生》2013年第10期1460-1462,共3页Chinese Journal of Public Health
基 金:辽宁省科技计划项目(2009225010-40);辽宁省教育厅创新团队项目(2009T064)
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。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-&alpha;(TNF-&alpha;)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-&alpha; 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).Conclusion Adenosine has a protective effect on LPS-induced cardiac hypertrophy.The mechanism may be related to the inhibition of TLR 4.
关 键 词:腺苷 脂多糖 炎症因子 肿瘤坏死因子(TNF-&alpha ) Toll样受体4(TLR4)
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