埃斯京能减轻糖尿病大鼠的心肌病 - NF-κβ 和 MCP-1 的可能作用

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-02-01 Epub Date: 2021-08-12 DOI:10.1080/13813455.2021.1963782

Sachin V Suryavanshi, Yogesh A Kulkarni

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引用次数: 0

摘要

目的：糖尿病心肌病是糖尿病最常见的并发症之一：糖尿病心肌病是糖尿病最常见的并发症之一。埃辛具有抑制 NF-κβ、抗糖尿病、神经保护和强效抗炎活性，可明显抑制心肌损伤。因此，本研究评估了埃辛对糖尿病心肌病的影响：方法：用链脲菌素诱导大鼠患糖尿病。方法：用链脲佐菌素诱导大鼠患糖尿病，诱导六周后，在接下来的四周内分别给糖尿病动物注射埃辛（5、10 和 20 毫克/千克）：结果：Escin 阻止了生化指标、血流动力学指标和心电图异常的发展。埃辛还阻止了氧化应激参数异常的进展。埃斯丁治疗后，NF-κβ和MCP-1的表达明显减少。此外，埃辛还能防止心肌细胞受损，减少心肌细胞中胶原蛋白的沉积：结论：埃丝菌素可预防糖尿病大鼠心肌病的恶化。因此，埃辛可以作为治疗糖尿病心肌病的替代选择。

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Abrogation of cardiomyopathy in diabetic rats by escin - possible role of NF-κβ and MCP-1.

Objective: Diabetic cardiomyopathy is one of the most common complications of diabetes. Escin may significantly inhibit myocardial damage through its NF-κβ inhibitory, antidiabetic, neuroprotective, and potent anti-inflammatory activity. Hence, the study was carried out to evaluate the effect of escin in diabetic cardiomyopathy.

Methods: Diabetes induction was done in rats with streptozotocin. After six weeks of induction, diabetic animals were administered with escin (5, 10, and 20 mg/kg) for the next four weeks.

Results: Escin prevented the progression of abnormalities in the biochemical, hemodynamic parameters and electrocardiogram. Escin also prevented the progression of abnormality in the oxidative stress parameters. The expression of NF-κβ and MCP-1 was significantly reduced with escin treatment. Furthermore, escin also prevented damage to myocardial cells and reduced collagen deposition in the cardiomyocytes.

Conclusion: Escin prevented the progression of cardiomyopathy in diabetic rats. Hence escin can be an alternative option for the management of diabetic cardiomyopathy.

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

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.