Aim: To study the relationship between P38MAPK and MCP-1 in diabetic HUVEC and the mechanism of anti-atherosclerosis of selenium.
Methods: HUVEC were treated with high concentration of glucose, advanced glycosylation end products (AGE), high concentration of insulin or H(2)O(2) with or without pre-treatment with SB203580 (P38MAPK specific inhibitor) or selenium. The expression of phospho-P38MAPK and MCP-1 in HUVEC was detected by Western blot or RT-PCR, respectively.
Results: High concentration of glucose, AGE, high concentration of insulin and H(2)O(2) can activate P38MAPK and increase the expression of MCP-1 in HUVEC. The expression of MCP-1 was inhibited by SB203580. Selenium inhibited the activation of P38MAPK and reduced the expression of MCP-1.
Conclusion: P38MAPK is an upstream signaling molecule of MCP-1. P38MAPK may be one of the initiating signals of diabetic atherosclerosis. Selenium can inhibit the expression of MCP-1 by repressing P38MAPK signaling pathway and therefore prevent the development of atherosclerosis.
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