| Objective:The present study conducted was to observe the effects of EM1/EM2on the human umbilical vein endothelial cells (HUVEC) caused by ox-LDL and to discuss the possible mechanism of it.Methods:HUVECs were treated with ox-LDL in the presence or absence of EM1/EM2. The MTT assay was used to assess the cell viability, colorimetric analysis was used to detect the levels of nitric oxide (NO) and nitric oxide synthase (NOS), and the enzyme-linked immunosorbent assay (ELISA) was used to measure endothelin-1(ET-1). Besides, reverse transcription polymerase chain reaction (RT-PCR) was adopted to detect the mNRA levels of eNOS, ET-land JNK, immunofuorescence to testify the protein expression of p-JNK in each group.Results:EM1/EM2prevented the decrease of the cell viability in the presence of and ox-LDL. Ox-LDL decreased the secretion of NO and NOS, which is consistent with the expression of eNOS mRNA, but the mRNA expression and secretion of ET-1had opposite changes. However, the above-mentioned findings would have opposite changes with the involvement of EM1/EM2. Meanwhile, the expression of JNK and p-JNK were enhanced by ox-LDL while suppressed by EM1/EM2.Conclusion:EM1/EM2is helpful for protecting decrease of cell viability induced by ox-LDL and the protective effect may be achieved by affecting the JNK pathway. |
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