Markers of Endogenous Intoxication in Rats with Diabetes Mellitus Combined with Carrageenan-Induced Enterocolitis

Q4 Medicine
І. Krynytska, M. Marushchak, Inna Birchenko, I. Klishch
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引用次数: 2

Abstract

Abstract Background and aims: Diabetes mellitus (DM) is a significant public health issue, being one of the major contributors to morbidity and mortality in the modern societies. Chronic hyperglycemia produces significant physiological, biochemical, and histological changes in the affected organisms. This study aims to evaluate the markers of endogenous intoxication in rats with diabetes mellitus combined with carrageenan-induced enterocolitis. Materials and methods: Diabetes mellitus was induced by a single intraperitoneal administration of streptozotocin (Sigma Aldrich, USA, at a dose of 60 mg/kg body weight). Carrageenan-induced enterocolitis was modeled by giving the animals free access to 1.0 % solution of carrageenan in drinking water for 1 month. The syndrome of endogenous intoxication was assessed by quantification of low and medium molecular weight substances in blood plasma, red blood cell suspension and urine using extraction-spectrophotometric method. Results: The increase in endogenous intoxication in streptozotocin-induced diabetes combined with chronic enterocolitis can mainly be attributed to the catabolic pool of blood plasma substances of low and medium molecular weight. The index of distribution of low- and medium-molecular-weight substances between blood plasma proteins and glycocalyx of erythrocytes in the experimental groups increased simultaneously with the quantities of investigated fractions in the erythrocyte suspension measured at the wavelengths of 242, 254 and 280 nm. Conclusions: We observed upsurge of endogenous intoxication markers in the rats with diabetes mellitus. Endotoxicosis became even more evident in the rats with diabetes mellitus combined with carrageenan-induced enterocolitis.
糖尿病合并卡拉胶性小肠结肠炎大鼠内源性中毒标志物的研究
背景与目的:糖尿病(DM)是一个重大的公共卫生问题,是现代社会发病率和死亡率的主要贡献者之一。慢性高血糖在受影响的生物体中产生显著的生理、生化和组织学变化。本研究旨在探讨糖尿病合并卡拉胶性小肠结肠炎大鼠内源性中毒的标志物。材料与方法:采用单次腹腔注射链脲佐菌素(Sigma Aldrich,美国,剂量为60 mg/kg体重)诱导糖尿病。通过在饮用水中加入1.0%的卡拉胶溶液1个月,建立了卡拉胶诱导的小肠结肠炎模型。采用提取-分光光度法定量测定血浆、红细胞悬浮液和尿液中低、中分子量物质,评价内源性中毒综合征。结果:链脲佐菌素所致糖尿病合并慢性小肠结肠炎患者内源性中毒的增加主要与血浆中、低分子量物质的分解代谢池有关。在242、254和280 nm波长下,实验组血浆蛋白与红细胞糖萼之间的中、低分子量物质分布指数随红细胞悬浮液中所测组分的数量同时增加。结论:糖尿病大鼠内源性中毒标志物升高。内毒素中毒在糖尿病合并卡拉胶诱导的小肠结肠炎的大鼠中更为明显。
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来源期刊
CiteScore
0.80
自引率
0.00%
发文量
49
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