Anti-diabetic effect of quercetin in type 2 diabetes mellitus by regulating the microRNA-92b-3p/EGR1 axis.

IF 2 4区 医学 Q3 PHYSIOLOGY
R Q Ke, Y Wang, S H Hong, L X Xiao
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引用次数: 0

Abstract

Insulin resistance (IR) is predominantly causal for type 2 diabetes mellitus (T2DM). To solve this problem, this study particularly determined the role of quercetin (Que) in controlling IR in T2DM mice. The T2DM mouse model was established, and given 20 mg/kg/d Que by gavage for 6 weeks, and the lentiviral vector that interfered with microRNA-92b-3p (miR-92b-3p) or early growth response 1 (EGR1) expression was injected into the tail vein of T2DM mice. Blood glucose homeostasis and histopathological changes in the pancreas were observed after the corresponding treatment. miR-92b-3p and EGR1 expressions were assessed in T2DM mice, as well as their interlink. In results we found that Que could improve IR and pancreatic histopathological changes in T2DM mice. Low miR-92b-3p and high EGR1 were expressed in T2DM mice, while Que could upregulate miR-92b-3p to target EGR1. Enhancing miR-92b-3p or reducing EGR1 could further improve IR and pancreatic histopathological changes in T2DM mice after Que administration. Nevertheless, silencing miR-92b-3p or overexpressing EGR1 contributed to the opposite results. We concluded that Que exerted anti-diabetic effects in T2DM mice by regulating the miR-92b-3p/EGR1 axis.

槲皮素通过调控microRNA-92b-3p/EGR1轴对2型糖尿病的降糖作用。
胰岛素抵抗(IR)是2型糖尿病(T2DM)的主要原因。为了解决这一问题,本研究特别确定了槲皮素(Que)在控制T2DM小鼠IR中的作用。建立T2DM小鼠模型,灌胃给药20 mg/kg/d Que,持续6周,将干扰microRNA-92b-3p (miR-92b-3p)或早期生长反应1 (EGR1)表达的慢病毒载体注入T2DM小鼠尾静脉。治疗后观察胰腺血糖稳态及组织病理变化。在T2DM小鼠中评估miR-92b-3p和EGR1的表达及其相互联系。结果发现,Que可以改善T2DM小鼠的IR和胰腺组织病理学改变。在T2DM小鼠中miR-92b-3p低表达,EGR1高表达,而Que可上调miR-92b-3p靶向EGR1。增强miR-92b-3p或降低EGR1可进一步改善T2DM小鼠给药后IR和胰腺组织病理学改变。然而,沉默miR-92b-3p或过表达EGR1会导致相反的结果。我们得出结论,Que通过调节miR-92b-3p/EGR1轴在T2DM小鼠中发挥抗糖尿病作用。
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来源期刊
CiteScore
4.00
自引率
22.70%
发文量
0
审稿时长
6-12 weeks
期刊介绍: Journal of Physiology and Pharmacology publishes papers which fall within the range of basic and applied physiology, pathophysiology and pharmacology. The papers should illustrate new physiological or pharmacological mechanisms at the level of the cell membrane, single cells, tissues or organs. Clinical studies, that are of fundamental importance and have a direct bearing on the pathophysiology will also be considered. Letters related to articles published in The Journal with topics of general professional interest are welcome.
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