2型糖尿病
下调和上调
基因沉默
小RNA
链脲佐菌素
内科学
医学
糖尿病
内分泌学
药理学
化学
生物化学
基因
作者
Ragovin Ke,Yanfang Wang,Seonki Hong,Ling Xiao
出处
期刊:PubMed
日期:2023-04-01
卷期号:74 (2)
被引量:5
标识
DOI:10.26402/jpp.2023.2.03
摘要
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.
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