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姜黄素对大鼠肠缺血再灌注损伤后肠道氧化应激、细胞增殖和细胞凋亡的作用。

The role of curcumin on intestinal oxidative stress, cell proliferation and apoptosis after ischemia/reperfusion injury in rats.

机构信息

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

出版信息

J Mol Histol. 2011 Dec;42(6):579-87. doi: 10.1007/s10735-011-9364-0. Epub 2011 Oct 8.

Abstract

The aim of this study was to demonstrate the role of curcumin 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+ curcumin; each group contain 10 animals. Sham group animals underwent laparotomy without I/R injury. After I/R groups animals underwent laparotomy, 1 h of superior mesenteric artery ligation were followed by 1 h of reperfusion. In the curcumin group, 3 days before I/R, curcumin (100 mg/kg) was administered by gastric gavage. All animals were sacrificed at the end of reperfusion and intestinal tissues samples were obtained for biochemical and histopathological investigation in all groups. Curcumin treatment significantly decreased the elevated tissue malondialdehyde levels and increased of reduced superoxide dismutase, and glutathione peroxidase enzyme activities in intestinal tissues samples. I/R caused severe histopathological injury including mucosal erosions and villous congestion and hemorrhage. Curcumin treatment significantly attenuated the severity of intestinal I/R injury, with inhibiting of I/R-induced apoptosis and cell proliferation. These results suggest that curcumin treatment has a protective effect against intestinal damage induced by intestinal I/R. This protective effect is possibly due to its ability to inhibit I/R-induced oxidative stress, apoptosis and cell proliferation.

摘要

本研究旨在探讨姜黄素对缺血再灌注(I/R)后大鼠肠黏膜氧化应激、细胞增殖和凋亡的作用。将 30 只雄性 Wistar 白化大鼠随机分为三组:假手术组、I/R 组和 I/R+姜黄素组,每组 10 只。假手术组动物仅行剖腹术,不进行 I/R 损伤。I/R 组动物行剖腹术后,结扎肠系膜上动脉 1 小时,再灌注 1 小时。在姜黄素组中,在 I/R 前 3 天,通过胃管给予姜黄素(100mg/kg)。所有动物在再灌注结束时处死,采集肠组织样本进行生化和组织病理学研究。姜黄素治疗可显著降低组织丙二醛水平升高,并增加肠组织样本中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,包括黏膜糜烂和绒毛充血和出血。姜黄素治疗可显著减轻 I/R 引起的肠损伤,抑制 I/R 诱导的细胞凋亡和增殖。这些结果表明,姜黄素治疗对 I/R 诱导的肠损伤具有保护作用。这种保护作用可能是由于其抑制 I/R 诱导的氧化应激、凋亡和细胞增殖的能力。

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