Role of RIP140 in the inhibition of curcumin on apoptosis in MIN6 cells

Objective To investigate the role of receptor interaction protein 140 (RIP140) in the inhibition of curcumin on apoptosis in MIN6 cells. Methods MIN6 cells were divided into five groups: control group, high glucose and lipid group, curcumin group, O-RIP140-MIN6 group (MIN6 cells with overexpressed RIP140) and GFP-MIN6 group (empty vector group). Except for control group, all other groups were treated with 25 mmol/L glucose and 500 μmol/L palmitic acid for 24 hours. Cells in curcumin group, O-RIP140-MIN6 group and GFP-MIN6 group were pretreated with 20 μmol/L curcumin for 2 hours before the treatment of 25 mmol/L glucose and 500 μmol/L palmitic acid for 24 hours. Apoptosis rate was detected by flow cytometry, the expression of B-cell lymphoma 2 (Bcl-2), extracellular regulated protein kinases (ERK) and phosphated-ERK were tested by Western blotting. Results Compared with control group, the expression of RIP140 protein, apoptosis rate and the level of phosphated-ERK were significantly increased whereas the expression of Bcl-2 was decreased in high glucose and lipid group (F=22.42-111.43, all P<0.01). However, compared with high glucose and lipid group, the apoptosis rate and the expression of RIP140 and phosphated-ERK were inhibited whereas the expression of Bcl-2 was increased in curcumin group(F=22.42-111.43, all P<0.01). Compared with GFP-MIN6 group, the apoptosis rate (t=7.16, P<0.01) and the level of phosphated-ERK(t=8.37, P<0.01) were increased and the expression of Bcl-2(t=5.88, P<0.05) was decreased in O-RIP140-MIN6 group. Conclusion Curcumin inhibits glucolipotoxicity-induced apoptosis in islet β cells via the downregulation of RIP140 expression. Key words: Receptor interaction protein 140; Curcumin; Islet β cells; Apoptosis