Fig. 8

mSMG-MS or berberine alleviated IR and promoted glycogen synthesis in IR-HepG2 cells, which may be related to the inhibition of TNF-α/JNK1/IRS-2 pathway. A Cell viability after treatment with different concentrations of mSMG-MS (0–40%) or berberine (0–250 μM) in IR-HepG2 cells for 4 h. B Glucose consumption of HepG2 cells after treatment with 5 μM insulin and 30 ng/mL TNF-α (IR), or 5 μM insulin and 30 ng/mL TNF-α added with 0.5 mM metformin or mSMG-MS (2.5–20%), or berberine (5–50 μM) for 4 h. 20% mSMG-MS or 50 μM berberine (C–E) improved glucose consumption, glycogen content, and glycogen synthase activity, F–H decreased the phosphorylation of JNK1 and IRS-2 (Ser³⁸⁸), and F, I–K increased phosphorylation of Akt (Ser⁴⁷³) and GSK-3β (Ser⁹) as well as the expression of GLUT2 protein in TNF-α-induced IR HepG2 cells. HepG2 cells were incubated for 4 h in medium containing blank (Control group), or 5 μM insulin and 30 ng/mL TNF-α (IR group), or 5 μM insulin and 30 ng/mL TNF-α added with 20%NS (NS group) or 20%MS (MS group) or 50 μM berberine (BBR group). Data are expressed as mean ± SD (n = 3, *P < 0.05, **P < 0.01, ***P < 0.001)