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[目的]探讨1,6-二磷酸果糖(FDP)对油酸致伤大鼠急性呼吸窘迫综合征治疗作用的可能机制。[方法]将30只健康的Wistar大鼠随机分为对照组、ARDS模型组、FDP治疗组,对照组:静脉注入生理盐水2.1ml/kg;ARDS模型组:注入油酸0.1ml/kg,然后注入生理盐水2.0ml/kg。FDP治疗组:注入油酸剂量和方法同上,然后注入用生理盐水稀释的FDP400mg/kg(2.0ml/kg)。3h后测定肺组织SOD,MDA,并计算左肺湿干重比值,行肺组织病理学观察。[结果]ARDS组与对照组比较,左肺湿干重比值、肺组织中MDA含量明显升高,而肺组织中SOD酶活性明显降低,肺组织出现明显病理损害,FDP治疗组动物肺损伤轻于模型组。[结论]FDP可抑制MDA升高,提高肺组织SOD酶活性,FDP对实验性大鼠油酸型急性呼吸窘迫综合征有一定的治疗作用。
[Objective] To investigate the possible mechanism of fructose 1,6-diphosphate (FDP) on acute respiratory distress syndrome induced by oleic acid in rats. [Methods] Thirty healthy Wistar rats were randomly divided into control group, ARDS model group, FDP treatment group and control group: normal saline 2.1ml / kg; ARDS model group: oleic acid 0.1ml / kg, then Injection of saline 2.0ml / kg. FDP treatment group: The oleic acid dose was injected and the method was the same as above, followed by injection of 400 mg / kg FDP diluted with physiological saline (2.0 ml / kg). 3h after the determination of SOD and MDA in lung tissue, and calculate the ratio of left lung wet and dry weight, lung pathological observation. [Results] Compared with the control group, the ratio of left lung wet weight to dry weight, the content of MDA in lung tissue were significantly increased in ARDS group and the SOD activity in lung tissue was significantly decreased, while the pathological damage in lung tissue was obvious. In the model group. [Conclusion] FDP can inhibit the increase of MDA, increase the activity of SOD in lung tissue, and FDP has a certain therapeutic effect on the experimental rat oleic acid-type acute respiratory distress syndrome.