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Protective effects of a free radical scavenger, MCI‐186, on high‐glucose–induced dysfunction of human dermal microvascular endothelial cells
Author(s) -
Jiaojun Dong,
Takami Yoshihiro,
Tanaka Hideharu,
Yamaguchi Ryo,
Jingping Guo,
Chun Qing,
ShuLiang Lu,
Shimazaki Shuji,
Ogo Ken
Publication year - 2004
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1067-1927.2004.12607.x
Subject(s) - apoptosis , mapk/erk pathway , free radical scavenger , endothelial stem cell , endothelial dysfunction , caspase 3 , endocrinology , medicine , chemistry , cell growth , cancer research , oxidative stress , microbiology and biotechnology , kinase , programmed cell death , biology , biochemistry , in vitro
Functional damage to microvascular endothelial cells by hyperglycemia is thought to be one of the critical risk factors in the impaired wound healing seen with diabetes mellitus. It is also thought that free radical stress plays a significant role in this endothelial cell dysfunction. In the present study, the effect of a free radical scavenger, MCI 186, on the endothelial cell dysfunction of cultured cells induced by high‐glucose conditions was studied. Human dermal microvascular endothelial cells were cultured with high‐glucose medium (50 mM) with or without MCI‐18 6 (10 μM) for 7 days. Fifty mM mannitol was used as an osmotic control in this study. After this treatment, cell proliferation, activation of mitogen‐activated protein kinase (MAPK), the level of apoptosis, and caspase‐3 activation induced by removal of growth factors or tumor necrosis factor‐α treatment were studied. High‐glucose conditions significantly decreased cell proliferation and increased apoptosis levels with the activation of caspase‐3 induced by growth factor removal. The high‐glucose condition significantly activated MAPK. MCI‐186 treatment improved cellular proliferation and reduced apoptosis and caspase‐3 activation induced by high‐glucose conditions. MCI‐186 also inhibited the activation of MAPK. On the other hand, MCI‐186 did not alter the level of apoptosis and caspase‐3 activation induced by TNF‐α treatment. In conclusion, we suggest that MCI‐186 may be beneficial for improving the endothelial cell dysfunction induced by hyperglycemia.