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英夫利昔单抗在大鼠肠缺血/再灌注损伤模型中的抗炎和抗氧化作用。

Anti-inflammatory and antioxidant effects of infliximab in a rat model of intestinal ischemia/reperfusion injury.

作者信息

Pergel Ahmet, Kanter Mehmet, Yucel Ahmet Fikret, Aydin Ibrahim, Erboga Mustafa, Guzel Ahmet

机构信息

Department of Surgery, Faculty of Medicine, Rize University, Rize, Turkey.

出版信息

Toxicol Ind Health. 2012 Nov;28(10):923-32. doi: 10.1177/0748233711427056. Epub 2011 Nov 14.

Abstract

The aim of this study was to investigate the possible protective effects of infliximab on oxidative stress, cell proliferation and apoptosis in the rat intestinal mucosa after ischemia/reperfusion (I/R). A total of 30 male Wistar albino rats were divided into three groups: sham, I/R and I/R+ infliximab; each group comprised 10 animals. Sham group animals underwent laparotomy without I/R injury. I/R groups after undergoing laparotomy, 1 hour of superior mesenteric artery ligation occurred, which was followed by 1 hour of reperfusion. In the infliximab group, 3 days before I/R, infliximab (3 mg/kg) was administered intravenously. All animals were killed at the end of reperfusion and intestinal tissues samples were obtained for biochemical and histopathological investigation in all groups. To date, no biochemical and histopathological changes have been reported regarding intestinal I/R injury in rats due to infliximab treatment. Infliximab treatment significantly decreased the elevated tissue malondialdehyde levels and increased reduced superoxide dismutase and glutathione peroxidase enzyme activities in intestinal tissues samples. I/R caused severe histopathological injury including mucosal erosions, inflammatory cell infiltration, necrosis, hemorrhage, and villous congestion. Infliximab treatment significantly attenuated the severity of intestinal I/R injury, inhibiting I/R-induced apoptosis, and cell proliferation. Because of its anti-inflammatory and antioxidant effects, infliximab pretreatment may have protective effects on the experimental intestinal I/R model of rats.

摘要

本研究旨在探讨英夫利昔单抗对大鼠肠缺血/再灌注(I/R)后肠黏膜氧化应激、细胞增殖和凋亡的可能保护作用。将30只雄性Wistar白化大鼠分为三组:假手术组、I/R组和I/R+英夫利昔单抗组;每组10只动物。假手术组动物仅行剖腹手术,无I/R损伤。I/R组动物剖腹手术后,进行1小时的肠系膜上动脉结扎,随后再灌注1小时。在英夫利昔单抗组中,在I/R前3天静脉注射英夫利昔单抗(3mg/kg)。再灌注结束时处死所有动物,并获取所有组的肠组织样本进行生化和组织病理学研究。迄今为止,尚未有关于英夫利昔单抗治疗大鼠肠I/R损伤的生化和组织病理学变化的报道。英夫利昔单抗治疗显著降低了肠组织样本中升高的丙二醛水平,并提高了超氧化物歧化酶和谷胱甘肽过氧化物酶的活性。I/R导致严重的组织病理学损伤,包括黏膜糜烂、炎性细胞浸润、坏死、出血和绒毛充血。英夫利昔单抗治疗显著减轻了肠I/R损伤的严重程度,抑制了I/R诱导的细胞凋亡和细胞增殖。由于其抗炎和抗氧化作用,英夫利昔单抗预处理可能对大鼠实验性肠I/R模型具有保护作用。

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