Protective Effect And Mechanism Of Resveratrol On Ages Injured Human Umbilical Vein Endothelial Cells

Background:In recent years, diabetes has become a serious health problem, which comes after cerebral vascular diseases and tumors. with the improve dliving standard and lifestyle changes, the prevalence of diabetes is higher and higher. The life quanlity of diabetes patients were affected by the complications. One of the most common chronic complications of diabetes is the macrovascular disease, the main cause of which is the endothelial dysfunction. Studies have shown that sustained high glucose can induce a variety of non enzymatic glycation of protein and then form advanced glycation end products (AGEs). It plays an important role in the development and progression of the chronic complications of diabetes. Advanced glycation end products (AGEs) can damage vascular endothelial cells, and lead to function disorders and physiological changes. Therefore, the development of drugs that can effectively protect vascular endothelial cell against the glycosylation injury is very important for the prevention and treatment of diabetic vascular complications.Resveratrol (Res), a natural plantibody produced under stress such as microbial infection, ultraviolet irradiation, belongs to non flavonoids polyphenolic compounds. In1940, it was first separated from the hair root of Veratrum grandiflorum by Japanese scientists. Then A lot of research has been done on Res and it is found that Res widely existed in Polygonum cuspidatum, grape, peanut, resveratrol and other plants. It is reported that Res has the activity of anti-tumor, cardiovascular protection, antioxidant, anti-inflammatory, antibacterial and antiviral effect, immune regulation etc.Objective:To investigate the protective effect and the possible mechanism of Resveratrol (Res) on human umbilical vein endothelial cells (HUVECs) injured by Advanced glycation end products (AGEs)Methods:The HUVEC incubated in AGE-modified bovine serum albumin (AGE-BSA) with a high concentration of glucose. HUVEC were divided into five groups:the control group, the AGEs group, the2.5μmol/L Res+AGEs group, the5μmol/L Res+AGEs group, and the10μmol/LRes+AGEs group. The cell proliferation of HUVEC, the concentration of cytoplasmic cytochrome C, the activity of caspase-3, and the expression of lactadherin mRNA were measured.Results:Compared with BSA group, the viability of HUVEC was significantly reduced (P<0.05) and the concentration of cytoplasmic cytochrome C, the activity of caspase-3, and the expression of lactadherin mRNA was increased (P<0.05) Compared with AGEs group, the cell viability of HUVEC treated with2.5,5,10μmol/L Res was increased (P<0.05) and the concentration of cytoplasmic cytochrome C, the activity of caspase-3, and the expression of lactadherin mRNA were decreased (P<0.05)Conclusion:AGEs could inhibit the cell viability of HUVEC. Res could protect HUVEC against the damage induced by AGEs and decrease the mRNA expression of lactadherin. The mechanism may be related to the decreasdexpression of lactadherin mRNA in HUVEC. This study provided the scientific basis for the development of Res as effective drug candidate for the prevention and treatment of diabetic vascular complications.