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探讨谷氨酰胺(Gln)对脂多糖(LPS)致大鼠心功能障碍的保护作用。雄性健康清洁级大鼠45只,随机分为对照组(NS5ml)15只、LPS组(10mg/kg)15只、Gln(1g/kg)治疗组15只,腹腔注药后24h测定平均血压(MAP)、左室收缩末期压力(LVESP)、左室压力上升及下降最大变化速率(±dp/dtmax)等心功能指标;观察心肌病理变化,并分别用RT-PCR及Western blot方法测定Toll样受体4(TLR4)、核因子κB(NF-κB)及TNF-αmRNA及蛋白表达;ELISA检测心肌TNF-α含量。结果显示:LPS增高大鼠心肌TLR4、NF-κB及TNF-α表达及心肌TNF-α含量,同时导致左室功能减退。Gln可下调心肌TLR4、NF-κB及TNF-α表达,使心肌TNF-α含量下降,并部分改善左室功能。提示Gln对LPS致心肌损伤具有一定保护作用,其机制之一可能与抑制TLR4-NF-κB信号转导通路有关。
To investigate the protective effect of glutamine (Gln) on cardiac dysfunction induced by lipopolysaccharide (LPS) in rats. Forty-five healthy male rats were randomly divided into control group (NS5ml) 15, LPS group (10mg / kg) 15, Gln (1g / kg) treatment group 15, 24h after intraperitoneal injection measured mean blood pressure (MAP), left ventricular end-systolic pressure (LVESP), left ventricular pressure and maximal rate of change (± dp / dtmax) were measured. Cardiac pathological changes were observed and Toll-like (TLR4), nuclear factor κB (NF-κB) and TNF-αmRNA and protein expression; The results showed that: LPS increased myocardial TLR4, NF-κB and TNF-α expression and myocardial TNF-α content, while leading to left ventricular dysfunction. Gln down-regulated the expression of TLR4, NF-κB and TNF-α in myocardium, decreased the content of TNF-α in myocardium and partially improved left ventricular function. These results suggest that Gln may play a protective role in myocardial injury induced by LPS, and one of the mechanisms may be related to the inhibition of TLR4-NF-κB signal transduction pathway.