Mailuoning prevents high-glucose-mediated human umbilical vein endothelial cells apoptosis

OBJECTIVE： To investigated the role of Mailuoning in the prevention of highglucosemediated cell apoptosis in human umbilical vein endothelial cells （HUVEC） and the mechanisms involved. METHODS： MTT assay was used to investigate cell viability, western blot was used to investigate pro tein expression, and flow cytometric detection technology was used to detect cell apoptosis. RESULTS： Exposure of HUVEC to high glucose （50 mM） significantly suppressed cell viability and increased cell apoptosis compared with normal glu cose （11 mM） （all P〈0.05）. However, Mailuoning pre vented highglucoseinduced HUVEC apoptosis in dosedependent manner. Further studies indicated that Mailuoning suppressed highglucoseinduced p38 mitogenactivated protein kinase phosphoryla tion, but had no effect on extracellular signalregu lated kinase 1/2 and Akt phosphorylation. CONCLUSION： Mailuoning can prevent highglu coseinduced HUVEC apoptosis by suppressing p38 activation.

OBJECTIVE: To investigated the role of Mailuoning in the prevention of high-glucose-mediated ce apoptosis in human umbilical vein endothelial cell (HUVEC) and the mechanisms involved. METHODS: MTT assay was used to investigate ce viability, western blot was used to investigate pro tein expression, and flow cytometric detection technology was used to detect cell apoptosis. RESULTS: Exposure of HUVEC to high glucose (50 mM) significantly suppressed cell viability and increased cell apoptosis compared with normal glu cose (11 mM) (all P<0.05). However, Mailuoning pre vented high-glucose-induced HUVEC apoptosis in dose-dependent manner. Further studies indicatedthat Mailuoning suppressed high-glucose-induced p38 mitogen-activated protein kinase phosphorylation, but had no effect on extracellular signal-regulated kinase 1/2 and Akt phosphorylation. CONCLUSION: Mailuoning can prevent high-glucose-induced HUVEC apoptosis by suppressing p38 activation.