ABSTRACT
Objective To study the mechanism of high glucose level underlying the dysfunction of HUVEC.Methods The HUVEC were divided into normal control group,mannitol control group,and high glucose (33 mmol/L) control group after they were isolated and cultured.Expression of RICTOR protein was detected by RT-PCR and Western blot respectively.RICTOR-transfected overexpressed adenovirus served as a high glucose adenovirus group and RICTOR-transfected AD-GFP served as a high glucose blank virus group.The phosphorylation of Akt and eNOS was detected by Western blot and the volume of released NO was measured with nitrate reductase.Results The expression level of RICTOR protein was significantly lower in high glucose control group than in normal control group (1.00±0.16 vs 2.69±0.07,P＜0.01) and was significantly higher in high glucose adenovirus group than in high glucose blank virus group (0.57±0.03 vs 0.29 ± 0.02,P＜0.01).The phosphorylation of Akt and eNOS was significantly higher and the volume of released NO from HUVEC was significantly larger in high glucose adenovirus group than in high glucose blank virus group (0.95±-0.05 vs 0.56±0.04,P＜0.01;0.97±0.05 vs 0.55±0.07,P＜0.01;0.85±0.06 vs 0.56±0.04,P＜0.05).Conclusion Upregulating the expression of RICTOR protein can improve high glucose-induced dysfunction of HUVEC.
ABSTRACT
Objective To study the mechanism of high glucose level underlying the dysfunction of HUVEC.Methods The HUVEC were divided into normal control group,mannitol control group,and high glucose (33 mmol/L) control group after they were isolated and cultured.Expression of RICTOR protein was detected by RT-PCR and Western blot respectively.RICTOR-transfected overexpressed adenovirus served as a high glucose adenovirus group and RICTOR-transfected AD-GFP served as a high glucose blank virus group.The phosphorylation of Akt and eNOS was detected by Western blot and the volume of released NO was measured with nitrate reductase.Results The expression level of RICTOR protein was significantly lower in high glucose control group than in normal control group (1.00±0.16 vs 2.69±0.07,P＜0.01) and was significantly higher in high glucose adenovirus group than in high glucose blank virus group (0.57±0.03 vs 0.29 ± 0.02,P＜0.01).The phosphorylation of Akt and eNOS was significantly higher and the volume of released NO from HUVEC was significantly larger in high glucose adenovirus group than in high glucose blank virus group (0.95±-0.05 vs 0.56±0.04,P＜0.01;0.97±0.05 vs 0.55±0.07,P＜0.01;0.85±0.06 vs 0.56±0.04,P＜0.05).Conclusion Upregulating the expression of RICTOR protein can improve high glucose-induced dysfunction of HUVEC.