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谷氨酰胺可预防门静脉高压模型中的氧化应激。

Glutamine prevents oxidative stress in a model of portal hypertension.

作者信息

Zabot Gilmara Pandolfo, Carvalhal Gustavo Franco, Marroni Norma Possa, Licks Francielli, Hartmann Renata Minuzzo, da Silva Vinícius Duval, Fillmann Henrique Sarubbi

机构信息

Gilmara Pandolfo Zabot, Gustavo Franco Carvalhal, Henrique Sarubbi Fillmann, Department of Surgery, School of Medicine, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, RS 90610-000, Brazil.

出版信息

World J Gastroenterol. 2017 Jul 7;23(25):4529-4537. doi: 10.3748/wjg.v23.i25.4529.

DOI:10.3748/wjg.v23.i25.4529
PMID:28740341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5504368/
Abstract

AIM

To evaluate the protective effects of glutamine in a model of portal hypertension (PH) induced by partial portal vein ligation (PPVL).

METHODS

Male Wistar rats were housed in a controlled environment and were allowed access to food and water . Twenty-four male Wistar rats were divided into four experimental groups: (1) control group (SO) - rats underwent exploratory laparotomy; (2) control + glutamine group (SO + G) - rats were subjected to laparotomy and were treated intraperitoneally with glutamine; (3) portal hypertension group (PPVL) - rats were subjected to PPVL; and (4) PPVL + glutamine group (PPVL + G) - rats were treated intraperitoneally with glutamine for seven days. Local injuries were determined by evaluating intestinal segments for oxidative stress using lipid peroxidation and the activities of glutathione peroxidase (GPx), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) after PPVL.

RESULTS

Lipid peroxidation of the membrane was increased in the animals subjected to PH ( < 0.01). However, the group that received glutamine for seven days after the PPVL procedure showed levels of lipid peroxidation similar to those of the control groups ( > 0.05). The activity of the antioxidant enzyme GTx was decreased in the gut of animals subjected to PH compared with that in the control group of animals not subjected to PH ( < 0.01). However, the group that received glutamine for seven days after the PPVL showed similar GTx activity to both the control groups not subjected to PH ( > 0.05). At least 10 random, non-overlapping images of each histological slide with 200 × magnification (44 pixel = 1 μm) were captured. The sum means of all areas, of each group were calculated. The mean areas of eNOS staining for both of the control groups were similar. The PPVL group showed the largest area of staining for eNOS. The PPVL + G group had the second highest amount of staining, but the mean value was much lower than that of the PPVL group ( < 0.01). For iNOS, the control (SO) and control + G (SO + G) groups showed similar areas of staining. The PPVL group contained the largest area of iNOS staining, followed by the PPVL + G group; however, this area was significantly smaller than that of the group that underwent PH without glutamine ( < 0.01).

CONCLUSION

Treatment with glutamine prevents gut mucosal injury after PH in rats.

摘要

目的

评估谷氨酰胺在部分门静脉结扎(PPVL)诱导的门静脉高压(PH)模型中的保护作用。

方法

将雄性Wistar大鼠饲养在可控环境中,给予食物和水。24只雄性Wistar大鼠分为四个实验组:(1)对照组(SO)——大鼠接受剖腹探查术;(2)对照+谷氨酰胺组(SO+G)——大鼠接受剖腹手术并腹腔注射谷氨酰胺;(3)门静脉高压组(PPVL)——大鼠接受PPVL;(4)PPVL+谷氨酰胺组(PPVL+G)——大鼠腹腔注射谷氨酰胺7天。通过评估PPVL后肠段的脂质过氧化以及谷胱甘肽过氧化物酶(GPx)、内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)的活性来确定局部损伤情况。

结果

PH组动物的膜脂质过氧化增加(<0.01)。然而,PPVL术后接受7天谷氨酰胺治疗的组显示脂质过氧化水平与对照组相似(>0.05)。与未接受PH的对照组动物相比,接受PH的动物肠道中抗氧化酶GTx的活性降低(<0.01)。然而,PPVL后接受7天谷氨酰胺治疗的组显示GTx活性与未接受PH的两个对照组相似(>0.05)。对每个组织学切片以200×放大倍数(44像素=1μm)随机采集至少10张不重叠的图像。计算每组所有区域的总和平均值。两个对照组的eNOS染色平均面积相似。PPVL组显示eNOS染色面积最大。PPVL+G组染色量第二高,但平均值远低于PPVL组(<0.01)。对于iNOS,对照组(SO)和对照+G组(SO+G)显示相似的染色面积。PPVL组iNOS染色面积最大,其次是PPVL+G组;然而,该面积明显小于未用谷氨酰胺进行PH的组(<0.01)。

结论

谷氨酰胺治疗可预防大鼠PH后的肠黏膜损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/cdeb54b1ddfa/WJG-23-4529-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/cd76afe7fbcf/WJG-23-4529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/fba360c5fb7d/WJG-23-4529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/2030c7dc4549/WJG-23-4529-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/285eca614750/WJG-23-4529-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/961fb2397886/WJG-23-4529-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/cdeb54b1ddfa/WJG-23-4529-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/cd76afe7fbcf/WJG-23-4529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/fba360c5fb7d/WJG-23-4529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/2030c7dc4549/WJG-23-4529-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/285eca614750/WJG-23-4529-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/961fb2397886/WJG-23-4529-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1317/5504368/cdeb54b1ddfa/WJG-23-4529-g006.jpg

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