Fig. 6

ADSC/GDM sEV restore insulin sensitivity to liver cells after Thbs1 pharmacological interference. A ADSC-GDM cells were treated with different concentrations of LSKL (0, 5 μM, 10 μM) for 72 h. sEV^AG, sEV^AG−L5 and sEV^AG−L10 were collected and identified by TEM and NTA. B The expression of Thbs1 in sEV^AG, sEV^AG−L5 and sEV^AG−L10 was identified by western blotting. C sEV^AG, sEV^AG−L5 and sEV^AG−L10 were co-cultured with AML12 for 24–96 h, and cell viability was detected by CCK8 assays. D sEV^AG, sEV^AG−L5 and sEV^AG−L10 were co-cultured with AML12 for 48 h, and cell apoptosis was detected by flow cytometry. E Glucose uptake of AML12 cells after insulin treatment was measured. F. sEV^AG, sEV^AG−L5 and sEV^AG−L10 were co-cultured with AML12 for 48 h, and the expression of phosphorylated Smad2 and total Smad2 protein was detected by western blotting. G, H RT-PCR and western blotting were used to detect the expression of ER stress related genes in AML12 cells. Statistical data were presented as mean ± standard deviation (SD); ns, no significance; *P < 0.05, **P < 0.01, ***P < 0.001