谷氨酰胺对脂多糖致大鼠心肌凋亡保护作用的研究

目的探讨谷氨酰胺（Gin）对脂多糖（LPS）致大鼠心肌凋亡的保护作用。方法选择雄性健康清洁级大鼠45只，随机分为对照组（Ns5m1）15只、LPS组（10mg／kg）15只和Gln（1g／kg）治疗组15只。大鼠腹腔注药后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及免疫组化方法测定心肌Bax、Bcl-2mRNA及蛋白表达；TUNEL检测心肌细胞凋亡水平；比色法测定Caspase-3活性。结果LPS可促进大鼠心肌细胞Bax、Bcl-2mRNA及蛋白表达，致Bcl-2／Bax降低；增强Caspase-3活性，使心肌细胞凋亡增加，伴心功能减退。Gin可使Bcl-2／Bax增高（两组分别为3．24±0．20、5．62±0．31，P=0．036），同时降低Caspase-3活性[（两组分别为（142．34±11．57）μmol／L、（94．50±8．91）μmol／L，P=O．027]，部分抑制心肌细胞凋亡[（两组凋亡率分别为（45．15±4．83）％、（23．24±3．64）％，P=O．048]，减轻心肌损伤，并部分改善心功能[两组±dp／dt一分别为（6534．76±138．51）mmHg／s、（7655．59±174．25）innlHg／s，P=-0．042]。结论Gln可部分抑制LPS致心肌凋亡作用，对LPS致心肌损伤具有一定保护作用。

Protective effect of glutamine on lipopolysaccharide-induced rat myocardial apoptosis

Objective To explore the protective effect of glutamine （Gln） on lipopolysaccharide （LPS）- induced rat myocardial apoptosis. Methods 45 clean grade healthy male rats were randomly divided into three groups： 15 in control group（NS 5 ml）, 15 in LPS group（10 mg/kg） and 15 in Gln treatment group（1 g/kg）. 24 h after the abdominal injection, the functional indexes of heart such as the mean arterial pressure（MAP）, left ven- tricular end systolic pressure（LVESP） and the maximum velocity of intraventricular pressure rise and decline （~dp/ dtmax） were examined. The pathological changes of myocardium were examed, and mRNA and the protein expression of Bax, Bcl-2 were measured by RT-PCR and immunohistochemistry, levels of myocardial apoptosis by TUNEL, and Caspase-3 activity by calorimetry. Results In LPS group, Bax, Bcl-2 mRNA and the protein expression in rat myoeardium were promoted and Bel-2/Bax declined, the activity of Caspase-3 were increased, with the in- creasing of myocardial apoptosis and the declining of cardiac function. In Gin group, Bcl-2/Bax increased, but the activity of Caspase-3 declined, myocardial apoptosis was partial inhibited, myocardial injury was reducted and car- diac function improved. Conclusion Gin could inhibit LPS-induced myocardial apoptosis partially and have the protective effect on LPS-induced myocardial injury.