Curcumin suppresses the effect of inflammation on proliferation and apoptosis of vascular endothelial cells

Objective To investigate the protective role of curcumin in the dysfunctional vascular endothelial cells induced by inflammation. Methods THP-1 cells were pretreated with 20 μmol/L curcumin under the condition of 25 mmol/L glucose and 500 μmol/L palmitic acid, while other groups received 25 mmol/L glucose and 500 μmol/L palmitic acid and dimethyl sulfoxide (DMSO), seperately. After 24 h treatment, the real time Polymerase Chain Reaction(PCR) was explored to detect the mRNA expression of receptor interaction protein 140(RIP140), tumor necrosis factor-α (TNF-α) and interleukin- 6 (IL-6), while the concentration of TNF-α and IL-6 in the supernatant was detected by the enzyme-linked immunosorbent assay (ELISA). Human umbilical vein endothelial cells (HUVECs) were incubated with the supernatant from the THP-1 in each group. The methodology of 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, flow cytometry and western-blot was applied to investigate the proliferation, apoptosis and the protein expression of phosphorylated extracellular regulated protein kinases (ERK) and B-cell lymphoma 2 (Bcl-2). Results The mRNA expression of RIP140, TNF-α and IL-6 in the THP-1 cells and the concentration of TNF-α and IL-6 in the supernatant were significantly higher when treated with 25 mmol/L glucose and 500 μmol/L palmitic acid, than those in the control group (t= 8.55, 9.44, 9.73, 16.01, 19.22 with all P<0.05). In the groups treated with 25 mmol/L glucose and 500 μmol/L palmitic acid, the pretreatment with curcumin significantly decreased the mRNA expression of RIP140, TNF-α and IL-6 in the THP-1 cells and the concentration of TNF-α and IL-6 in the supernatant(t=3.59, 5.96, 5.59, 6.95, 23.91 with all P<0.05). At 24 h and 48 h treatment, compared with the control group, the supertant from the groups treated with 25 mmol/L glucose and 500 μmol/L palmitic acid significantly suppressed the proliferation of HUVECs (24 h: 1.22±0.07 vs 1.85±0.14, t=6.58, P<0.05; 48 h: 1.72±0.02 vs 2.49±0.09, t=10.08, P<0.05), while the proliferation of HUVECs could be improved by the pretreatment with 20 μmol/L curcumin (24 h: 1.22±0.07 vs 1.72±0.11, t=2.13, P<0.05; 48 h: 1.72±0.02 vs 2.33±0.11, t=6.92, P<0.05). Compared with the control group, the incubation with the supertant from the groups treated with 25 mmol/L glucose and 500 μmol/L palmitic acid significantly increased the apoptosis rate and the level of phosphated ERK, while decreased the Bcl-2 protein expression (t=9.82, 9.69, 4.61, all P<0.05). Such effect could be reserved by the pretreatment with 20 μmol/L curcumin (t=6.35, 7.17, 3.26, all P<0.05). Conclusion Curcumin could protect the vascular endothelial cells from the dysfunction induced by inflammation. Key words: Curcumin; Receptor interaction protein 140; Inflammation; Vascular endothelial cells