miR‑223‑3p reduces high glucose and high fat‑induced endothelial cell injury in diabetic mice by regulating NLRP3 expression
- Bo Deng
- Ying Hu
- Xia Sheng
- Huijun Zeng
- Yanan Huo
Affiliations: Department of Endocrinology, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China, Department of Pharmacy, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330008, P.R. China, Department of Endocrinology, Jiangxi Provincial People's Hospital, Nanchang, Jiangxi 330006, P.R. China
- Published online on: June 10, 2020 https://doi.org/10.3892/etm.2020.8864
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Expression levels of miR‑223‑3p and NLRP3 in high glucose and high fat (HGHF)‑induced diabetic mice, and the mechanism on the injury of mouse cardiac microvascular endothelial cells (MCMECs) were investigated. Four‑week C57BL/6J laboratory mice were selected and randomized into a control group and a model group (n=10 each). Mice in the model group were fed with HGHF diet to establish a mouse model of diabetes. Further MCMECs were purchased to construct carriers through transient transfection, and were separated into a normal group (cultured in the normal environment), a model group (not transfected), a blank carrier group (transfected with miR‑NC), a miR‑223‑3p‑mimics group, and a miR‑223‑3p‑inhibitor group. RT‑qPCR was used to detect the expression levels of miR‑223‑3p and NLRP3, and western blot analysis to detect the expression levels of NLRP3, apoptosis‑related proteins Bax and caspase‑3, and anti‑apoptotic protein Bcl‑2. Flow cytometry was used to observe apoptosis and TargetScan to predict the target relationship between miR‑223‑3p and NLRP3. Dual‑luciferase reporter gene assay was used to detect the relationship between miR‑223‑3p and NLRP3. Compared with those in the control group, the mice in the model group had significantly lower expression of miR‑223‑3p. However, significantly higher mRNA and protein expression levels of NLRP3 were observed (P<0.05). After modeling, miR‑223‑3p overexpression downregulated the expression levels of NLRP3 mRNA, Bax and NLRP3 protein, as well as inhibited endothelial cell apoptosis (P<0.05), while the inhibition of miR‑223‑3p expression upregulated the expression levels and promoted apoptosis. In conclusion, miR‑223‑3p expression is low, however, NLRP3 is highly expressed in the heart tissue of HGHF‑induced diabetic mice. miR‑223‑3p reduces the injury of MCMECs and inhibits endothelial cell apoptosis in mice by regulating the expression of NLRP3.