Naringenin ameliorates insulin resistance in HepG2 cells by regulating high miR - 29b expression

Acta Universitatis Medicinalis Anhui 2024 08 v.59 1423-1428     font:big middle small

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Authors:Wang Yuan; Zeng Kaihong; Yu Xuemei; Deng Bo

Keywords:naringenin;insulin resistance;microRNA-29b

DOI:10.19405/j.cnki.issn1000-1492.2024.08.020

〔Abstract〕 Objective To investigate the impact of naringenin(Nar) on insulin resistance(IR) in HepG2 cells and evaluate the role ofmircoRNA-29b(miR-29b) expression in mediating this effect, thereby providing a foundation for further exploration into the mechanisms underlying naringenin's 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 mimicand inhibitor were transfected into IR-HepG2 cells of the 50 μg/ml Nar intervention group, and the expressions of insulin receptor 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 expressions ofIRS-1andAktwere increased in Nar intervention group with different concentrations(P<0.05), the mRNA expression ofIRS-1andAktin 50 μg/ml Nar intervention group was the most significantly increased(P<0.001), andGLUT4mRNA expression in 50 μg/ml Nar intervention group was increased(P<0.05). The protein expressions ofIRS-1andp-Aktwere increased in different Nar concentration groups(P<0.001). Compared with IR-HepG2 model group, mRNA expression ofIRS-1,AktandGLUT4and protein expression of IRS-1 and p-Akt were decreased inmiR-29b mimictransfected cells(P<0.001), mRNA expression ofIRS-1,AktandGLUT4and protein expression of IRS-1 and p-Akt were not different inmiR-29b inhibitortransfection group, Nar intervention model group and Nar intervention transfectedmiR-29b mimicgroup increased the mRNA expression ofIRS-1,AktandGLUT4(P<0.001), and the protein expression of IRS-1 and p-Akt increased(P<0.05). Compared with Nar intervention model group, Nar transfectedmiR-29b mimicwith Nar intervention did not change the mRNA expressions ofIRS-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 inmiR-29b inhibitorgroup(P<0.001). Conclusion Nar can increase glucose consumption in IR-HepG2 cells, increase the expression ofIRS-1,AktandGLUT4genes, 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 overexpression ofmiR-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.