Ginsenoside Rg1 protects pancreatic INS-1 cell survival in β-cell through the PI3K/Akt signaling pathway

Background: Ginsenoside Rg1 possesses anti-diabetic properties. As a safe natural plant extraction, Ginsenoside Rg1 might serve as a preventive and/or therapeutic approach for diabetes, whether it acts directly on pancreatic β-cell is not clear. Purpose: Ginsenoside Rg1 protection of β-cell survival involved the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. In conclusion, Ginsenoside Rg1 protects pancreatic β-cell function and survival via direct effects on β-cells, and its protection of β-cell survival is mediated by the PI3K/Akt pathway. Materials and methods: The function of INS-1 cell proliferation was determined using 5-ethynyl-2′-deoxyuridine (EdU), Cell Counting Kit-8 (CCK-8).quantitative real-time PCR (RT-PCR) and Western blotting were performed to quantify AKT,PI3K,Ccnd1,Ccnd2,Cdk4 And Ki67 expression in INS-1 samples. Results: AKT, PI3K, Ccnd1, Ccnd2, Cdk4 And Ki67 was abnormally expressed in INS-1 samples compared with matched paired normal tissues. Inhibition of AKT/PI3K expression by(LY294002, cell Signaling)significantly inhibited proliferation of INS-1 cells. Further in vitro experiments indicated that led to lower expression of AKT/PI3K significantly reversed the inhibition of proliferation caused by Ginsenoside Rg1. Conclusion: Ginsenoside rg1 promoted Ins-1 cell proliferation via the AKT/PI3K.