Naringenin ameliorates insulin resistance in HepG2 cells by regulating high miR-29b expression
10.19405/j.cnki.issn1000-1492.2024.08.020
- Author:
Yuan Wang
1
,
2
;
Kaihong Zeng
3
,
4
;
Xuemei Yu
1
;
Bo Deng
1
Author Information
1. Dept of Clinical Nutrition,Sichuan Academy of Medical Sciences & Sichuan Provincial People s Hospital,Chengdu 610072
2. School of Medicine,University of Electronic Science and Technology of China, Chengdu 610054
3. School of Medicine,University of Electronic Science and Technology of China, Chengdu 610054
4. Dept of Health Management Center and Institute of Health Management,Sichuan Provincial People Hospital,University of Electronic Science and Technology of China,Chengdu 610072
- Publication Type:Journal Article
- Keywords:
naringenin;
insulin resistance;
microRNA-29b
- From:
Acta Universitatis Medicinalis Anhui
2024;59(8):1423-1428
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the impact of naringenin(Nar) on insulin resistance(IR) in HepG2 cells and evaluate the role of mircoRNA-29b (miR-29b) expression in mediating this effect,thereby providing a foundation for further exploration into the mechanisms underlying naringenin potential as a preventative and therapeutic agent for diabetes.
Methods :Insulin resistant HepG2 (IR-HepG2) was established by stimulating HepG2 cells with 100 nmol / L insulin.Nar was treated with different concentrations (0,25,50,100 μg / ml) in IR-HepG2 cells.The effect of Nar on glucose consumption in IR-HepG2 cells was determined with glucose kit.miR-29b mimic and inhib- itor were transfected into IR-HepG2 cells of the 50 μg / ml Nar intervention group,and the expressions of insulin re- ceptor substrate-1 (IRS-1) ,protein kinase B(Akt) / phosphorylated Akt (p-Akt) ,glucose transporter-4 ( GLUT4) genes and proteins in the insulin signaling pathway were detected by Real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot,respectively.
Results :Compared with IR- HepG2 model group,glucose consumption was increased in Nar intervention group with different concentrations (P <0. 01) ,among which 50 μg / ml Nar intervention group was the most significant (P <0. 001) ,and mRNA ex- pressions of IRS-1 and Akt were increased in Nar intervention group with different concentrations (P<0. 05) ,the mRNA expression of IRS-1 and Akt in 50 μg / ml Nar intervention group was the most significantly increased (P < 0. 001) ,and GLUT4 mRNA expression in 50 μg / ml Nar intervention group was increased (P<0. 05) .The pro- tein expressions of IRS-1 and p-Akt were increased in different Nar concentration groups (P <0. 001) .Compared with IR-HepG2 model group,mRNA expression of IRS-1,Akt and GLUT4 and protein expression of IRS-1 and p- Akt were decreased in miR-29b mimic transfected cells (P<0. 001) ,mRNA expression of IRS-1,Akt and GLUT4 and protein expression of IRS-1 and p-Akt were not different in miR-29b inhibitor transfection group,Nar interven- tion model group and Nar intervention transfected miR-29b mimic group increased the mRNA expression of IRS-1, Akt and GLUT4 (P <0. 001) ,and the protein expression of IRS-1 and p-Akt increased (P <0. 05 ) . Compared with Nar intervention model group,Nar transfected miR-29b mimic with Nar intervention did not change the mRNA expressions of IRS-1,Akt and GLUT4 ,while the protein expressions of IRS-1 and p-Akt were increased ( P < 0. 05 ) ,Nar interfered with mRNA expression of IRS-1,Akt and GLUT4 and protein expression of IRS-1 and p-Akt in miR-29b inhibitor group (P<0. 001) .
Conclusion :Nar can increase glucose consumption in IR-HepG2 cells, increase the expression of IRS-1,Akt and GLUT4 genes,and increase the expression of IRS-1 and p-Akt proteins in IR-HepG2 cells.Nar increases the expression of IRS-1 and p-Akt in IR-HepG2 cells by inhibiting the overexpres- sion of miR-29b,and improves insulin resistance in HepG2 cells.Nar,as a plant compound,is expected to be a potential drug for the prevention and treatment of diabetes.
- Full text:2024091415222439689柚皮素通过调控miR-29...2细胞胰岛素抵抗的改善作用_王元.pdf