Basic & Clinical Medicine ›› 2013, Vol. 33 ›› Issue (11): 1422-1425.

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Probucol inhibits NF-κB activation and ICAM-1 expression in human dermal fibroblasts induced by advanced glycation end products

1,Dian-Bao ZHANGping SHI1,Xiao-Yu LIU3,   

  • Received:2013-08-27 Revised:2013-09-17 Online:2013-11-05 Published:2013-10-28

Abstract: Objective To investigate the influence of Probucol on the activation of NF –κB and expression of ICAM-1 in dermal fibroblasts induced by advanced glycation end products (AGEs). Methods Fibroblasts were isolated and cultured in vitro, and then divided into 4 groups: control group, AGE-BSA group, low Probucol group(50μmol /L Probucol+100 mg /L AGE-BSA)and high Probucol group(100μmol /L Probucol+100 mg /L AGE-BSA).The content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) in Fibroblasts were detected. The Protein levels of NF – κB p65 and ICAM-1 were also measured by Western blot. Results (1) Compared with control group, the content of malondialdehyde (MDA) markedly was increased, the activities of superoxide dismutase (SOD) markedly were decreased in AGE-BSA group, the Protein levels of NF – κB P65 and ICAM-1 were markedly increased in AGE-BSA group. (2) Probucol markedly inhibited the decrease in SOD activity, the increase in the content of MDA in fibroblasts induced by AGE-BSA. In addition, the over-expression of NF–κB p65 and ICAM-1 in fibroblasts was inhibited markedly by Probucol. Conclusion Protective effect of probucol on dysfunction of fibroblasts induced by AGEs may be related with its effect on the suppressing the activation of NF–κB and subsequent expression of ICAM-1.

Key words: Probucol, advanced glycation end products, fibroblasts, Intercellular adhesion molecule-1