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Protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury after hemorrhagic shock in rats

机译:黄芪对失血性休克大鼠肠黏膜再灌注损伤的保护作用

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摘要

AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats.METHODS: A total of 32 SD rats were randomly divided into four groups (n = 8, each group): normal group, model group, low dosage group (treated with 10 g/kg Astragalus membranaceus) and high dosage group (treated with 20 g/kg Astragalus membranaceus). The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution (3 mL) was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid (LD), nitric oxide (NO), endothelin-1 (ET-1), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) in intestinal mucosa were determined.RESULTS: The intestinal mucosa pathology showed severe damage in model group and low dosage group, slight damage in high dosage group and no obvious damage in normal group. The Chiu’s score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group.CONCLUSION: High dose Astragalus membranaeus has much better protective effect on hemorrhagic shock-reperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.
机译:目的:研究黄芪对大鼠失血性休克后肠粘膜再灌注损伤的保护作用及其机制。方法:将32只SD大鼠随机分为4组(每组8只):正常组,每组8只。模型组,低剂量组(用10 g / kg黄芪治疗)和高剂量组(用20 g / kg黄芪治疗)。建立了失血性休克60分钟,再灌注90分钟的模型。在再灌注之前施用治疗溶液(3mL)。在研究结束时,对观察到的肠道病理进行了分析。肠道粘膜的血中乳酸(LD),一氧化氮(NO),内皮素-1(ET-1),丙二醛(MDA)的浓度以及超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-PX)的活性分别为结果:模型组和低剂量组肠黏膜病理表现为严重损伤,高剂量组肠黏膜病理损伤较轻,正常组无明显损伤。低剂量组和高剂量组的Chiu得分均显着低于模型组。模型组MDA含量高于低,高剂量组,而高剂量组与正常组几乎相同。 SOD和GSH-PX的活性在模型组中最低,在高剂量组中明显高于正常和低剂量组。模型组LD和ET-1浓度最高。结论:高剂量黄芪对小肠黏膜失血性休克再灌注损伤的保护作用优于低剂量黄芪。结论:高剂量黄芪对小肠黏膜失血性休克再灌注损伤具有更好的保护作用。其机制可能是黄芪在出血性再灌注过程中可以提高抗氧化作用并调节NO / ET水平。

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