外源性胃泌素对脂肪喂养链脲佐菌素大鼠模型氧化应激、炎症和组织学参数的影响

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Ozlem Ergul Erkec, Zubeyir Huyut, Eda Acikgoz, Mehmet Tahir Huyut
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引用次数: 0

摘要

本研究调查了胃泌素在脂肪喂养的链脲佐菌素(STZ)大鼠模型中的抗炎、抗氧化和保护作用,并与二甲双胍、糖尿病和健康对照组进行了比较。对 H&E 染色的胰腺和大脑切片进行了组织病理学评估。生化指标通过酶联免疫吸附试验进行检测。胃泌素或二甲双胍治疗组的血糖水平明显低于糖尿病组。STZ 会增加脑、肾和胰腺的 IL-1β、TNF-α 和 MDA,同时降低 GPX、CAT、SOD 和 NGF 水平。胃泌素能增加肾脏 GPX、CAT、NGF、胰腺 GPX、SOD、CAT、NGF 和脑部 SOD、NGF,同时降低肾脏、胰腺和脑部 IL-1β、TNF-α 和 MDA 水平。胃泌素减少了大脑皮层和海马的神经元损失和退化,并大大改善了糖尿病对胰腺的损害。总之,这些数据表明,胃泌素是减少糖尿病不良影响的有效候选保护剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of exogenous ghrelin treatment on oxidative stress, inflammation and histological parameters in a fat-fed streptozotocin rat model.

In this study, the anti-inflammatory, antioxidative, and protective effects of ghrelin were investigated in a fat-fed streptozotocin (STZ) rat model and compared with metformin, diabetes and the healthy control groups. Histopathological evaluations were performed on H&E-stained pancreas and brain sections. Biochemical parameters were investigated by enzyme-linked immunosorbent assay. Blood glucose levels were significantly decreased with ghrelin or metformin treatments than the diabetes group. STZ administration increased brain, renal and pancreatic IL-1β, TNF-α and MDA while decreasing GPX, CAT, SOD, and NGF levels. Ghrelin increased renal GPX, CAT, NGF pancreatic GPX, SOD, CAT, NGF and brain SOD, NGF while it decreased renal, pancreatic and brain IL-1β, TNF-α and MDA levels. Ghrelin reduced neuronal loss and degeneration in the cerebral cortex and hippocampus and greatly ameliorated diabetes-related damage in pancreas. In conclusion, the data suggested that ghrelin is an effective candidate as a protectant for reducing the adverse effects of diabetes.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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