Role of Baicalein combined with U0126 resisting human bladder carcinoma cell in vitro and mechanism research / 中国免疫学杂志

Objective:To investigate the role of Baicalein combined with U0126 resisting human bladder cancer T-24 cells in vitro and mechanism.Methods: T-24 cells were dealt with Baicalein combined with U0126,flow cytometry was used to detect cell cycle and cell apoptosis,microscope to count cell number,TUNEL method to detects cell apoptosis index,and Real time quantitative PCR and Western blot to measure extracellular signal regulating kinase 1/2 (ERK1/2), CyclinD1, GSK-3β and AKT RNA level, protein level of T-24 cells respectively.Effect of Baicalein and U0126 on apoptosis and proliferation of bladder cancer cell was analyzed.Results: Cell apoptosis rate was significantly increased after T-24 cells dealt with various concentrations of Baicalein.Cell proportion of G0/G1 phase was significantly increased,while cell percentage of S phase was obviously decreased and cell count was decreased,after T-24 cells were dealt with Baicalein for 24 h.After T-24 cells were dealt with Baicalein combined with U0126 for 24 h,cell proportion of S phase was evidently decreased.T-24 cells were dealt with Baicalein or U0126 obviously promoted cell apoptosis,which was more obvious with Baicalein combined with U0126.Phosphorylation level of GSK-3β,ERK1/2,and AKT was significantly reduced and expression of ERK1/2 and CyclinD1 mRNA was evidently lower after Baicalein or U0126 or Baicalein combined with U0126,and combined application had more remarkable effect.Conclusion: Baicalein and U0126 can induce apoptosis of T-24 cells,increase cell proportion in G0/G1 phase,reduce cell proportion of S phase,and Baicalein combined with U0126 effect has more remarkable effect.

Visfatin inhibits pancreatic β-cell line MIN6 apoptosis via PI3K-Akt and MAPK-ERK1/2 signaling pathways / 中华内分泌代谢杂志

To investigate the effects and the mechanism of visfatin on MIN6 cell signaling pathway and apoptosis induced by palmitate.Human recombinant visfatin promotes protein kinase B (Akt) and extracellularsignal regulating kinase (ERK)1/2 phosphorylation in dose-and time-dependent manner,and prevents MIN6 cell from apoptosis induced by palmitate (P<0.05 or P<0.01).The activation of Akt and ERK1/2 signaling pathway may be one of the molecular mechanisms of visfatin.