OBJECTIVE: To investigate the effects of tetramethylpyrazine on lipopolysaccharides (LPS)-induced expression of vascular endothelial growth factor (VEGF) and hypoxia-induced factor-1alpha (HIF-1alpha) in macrophages. METHOD: Rat peritoneal macrophages were treated with LPS, and at the same time given different doses of tetramethylpyrazine. The secreation of VEGF was determined by ELISA test, and MTT assay was used to examine cells proliferation. Western blot assay was used to examine the expression of HIF-1alpha. RESULT: 100 microg x mL(-1) and 10 microg x mL(-1) tetramethylpyrazine decreased the secretion of VEGF and also inhibited the expression of HIF-1alpha by LPS-induced macrophages. But these doses of tetramethylpyrazine had no effect on the cells proliferation. CONCLUSION: Tetramethylpyrazine could inhibit the secretion of VEGF by LPS-induced macrophages, and the mechanism must be associated with inhibiting the expression of HIF-1alpha. The inhibition effect was not due to inhibition of the proliferation of macrophages.
OBJECTIVE: To investigate the effects of tetramethylpyrazine on lipopolysaccharides (LPS)-induced expression of vascular endothelial growth factor (VEGF) and hypoxia-induced factor-1alpha (HIF-1alpha) in macrophages. METHOD:Rat peritoneal macrophages were treated with LPS, and at the same time given different doses of tetramethylpyrazine. The secreation of VEGF was determined by ELISA test, and MTT assay was used to examine cells proliferation. Western blot assay was used to examine the expression of HIF-1alpha. RESULT: 100 microg x mL(-1) and 10 microg x mL(-1) tetramethylpyrazine decreased the secretion of VEGF and also inhibited the expression of HIF-1alpha by LPS-induced macrophages. But these doses of tetramethylpyrazine had no effect on the cells proliferation. CONCLUSION:Tetramethylpyrazine could inhibit the secretion of VEGF by LPS-induced macrophages, and the mechanism must be associated with inhibiting the expression of HIF-1alpha. The inhibition effect was not due to inhibition of the proliferation of macrophages.