Objective To investigate the protective effect and its potential molecular mechanism of Nec-1 on cytotoxicity induced by cyclosporine A.Methods MRTEpiC, glomerular endothelial cell MGEC and mesangial cell line MMC were co-administered with Nec-1 and cyclosporin A in mouse renal tubular epithelial cell line, and then MTT assay and soft agar clone formation assay were used to detect Cell growth curve changes, clonal formation ability.Apoptosis was detected by flow cytometry.The expression of cyclin D1, CDK4, CDK2, Cyclin E and apoptosis-related Caspase 3 were detected by Western blot.Results After cyclosporine A action, the cell growth ability was significantly decreased and the clone formation ability was significantly decreased(P<0.05).Cyclin D1, CDK4, CDK2 and Cyclin E were significantly increased(P<0.05), but the ratio of apoptosis and the expression of Caspase 3 did not change.Nec-1 has obvious protective effect on cytotoxicity induced by cyclosporine A, which can increase the cell growth ability and clone formation ability, and reduce the cell cycle-related proteins Cyclin D1, CDK4, CDK2, Cyclin E.Conclusion Nec-1 has cytotoxic effect on the glomeruli and renal tubular cells by up-regulating the cell cycle-related proteins Cyclin D1, CDK4, CDK2 and Cyclin E, while Nec-1 has protective effect.

AIM: To investigate the effect of nobiletin (Nob) on cardiomyocyte hypertrophy induced by high glucose and its mechanism. METHODS: Neonatal rat cardiomyocytes (NRCMS) were stimulated with high glucose (HG) to establish cardiomyocyte hypertrophy and nobiletin was given. Cell viability was measured by MTT assay. C-myc and Nppa mRNA levels were detected by qRT-PCR. Cellular surface area was detected by immunofluorescence, and Nrf2 and HO-1 protein expressions were detected by Western blot. RESULTS: After stimulation with 33.3 mmol/L HG for 48 h, the survival rate of NRCMS was significantly decreased, C-myc, Nppa mRNA levels and cellular surface area were significantly increased, Nrf2 and HO-1 protein expression were significantly decreased (P<0.05). After Nob treatment, compared with HG group, cellular surface area, Nrf2 and HO-1 protein expression were significantly increased, C-myc and Nppa mRNA levels were significantly decreased. The above indexes were reversed by using Nrf2 inhibitor. CONCLUSION: Nob inhibits cardiomyocyte hypertrophy induced by high glucose, and its mechanism may be related to the activation of Nrf2/HO-1 signaling pathway.