Adiponectin suppresses inflammatory responses at the early phase of atherosclerosis in hyperglycemic rats.

Adiponectin plays an important role in atherosclerosis, but its relationship with the early initiation of atherosclerosis in diabetes mellitus is still not completely understood. In this study, we defined the role of adiponectin early in the process of atherosclerosis in hyperglycemic rats. Recombinant adenovirus expressing the full-length apM1 cDNA gene (Ad-APN) was constructed and successfully transfected into hyperglycemic rats characterized by the presentation of early atherosclerosis. The levels of sICAM-1 and C-reactive protein (CRP) in serum as well as the expression of VCAM-1, ICAM-1 and MCP-1 in aortic tissue were evaluated. Serum adiponectin was significantly increased in Ad-APN-treated rats compared with Ad-ßgal-treated rats. The levels of sICAM-1 and CRP in serum were dramatically reduced by 22 and 21%, respectively, in Ad-APN-treated rats. Additionally, in aortic tissue, significantly reduced mRNA levels of VCAM-1, ICAM-1 and MCP-1 were observed after Ad-APN transfection. These results suggest that, in hyperglycemic rats, adiponectin plays an inhibitory role in the early development of atherosclerosis. In conclusion, the protective effect of adiponectin is associated with the reduced activity of various inflammation-related factors.

[Study on the effect and mechanism of ascorbic acid on renal podocytes in diabetes].

AIM: To investigate the effect and mechanism of ascorbic acid on podocyte, last barrier of glomerular filtration, in diabetic rats. METHODS: Diabetic rats induced by streptozotocin injection intraperitoneally were treated by ascorbic acid for 5 weeks. The levels of blood glucose (BG), HbA1c, urinary albumin excretion rate (UAER) and superoxide diamutase (SOD), catalase (CAT) and malondialdehyde (MDA) in renal cortex were measured. The podocyte ultrastructure was observed while the expression of desmin protein, a marker of podocyte injury, was examined. RESULTS: Compared with control group, BG and HbA1c were increased markedly in diabetic group. The activities of SOD and CAT were decreased and the concentrations of MDA were increased significantly in diabetic renal cortex. There were the increased proteinic expression of desmin, foot process effacement in podocytes and UAER markedly in diabetic rats. Compared with diabetic rats, foot process effacement and the changes of UAER were ameliorated markedly while the activities of SOD were increased, the levels of MDA and proteinic expression of desmin were decreased markedly although BG, HbA1c and the activities of CAT were no significant difference in the diabetic rats by ascorbic acid treatment. CONCLUSION: The findings suggest that there are marked injury in podocyte, last barrier of glomerular filtration, in diabetic rats and administration of ascorbic acid can protect podocyte by increasing antioxidative capacity and ameliorating the renal oxidative stress.

[Effects of recombinant adenovirus encoding human apM1 gene on proliferation and nitric oxide synthase activity in human umbilical vein endothelial cells].

OBJECTIVE: To evaluate the effects of recombinant adenovirus encoding human apM1 gene on proliferation and nitric oxide synthase (NOS) activity in human umbilical vein endothelial cells (HUVECs). METHODS: Protein expression of apM1 in cell culture supernatant of HUVECs transfected with human Ad-apM1 was detected by double antibody sandwich ELISA. The effect of human adiponectin on cell proliferation was assessed by MTT assay. The total NOS and iNOS expressions were measured by chromatometre. RESULTS: Human adiponectin protein level and total NOS and eNOS expressions were significant increased and iNOS expression significantly reduced in culture supernatant of HUVECs infected with Ad-apM1 compared to that in control HUVECs. The recombinant adenovirus had no influence on HUVECs growth as determined by MTT assay. CONCLUSIONS: Human Ad-apM1 can be effectively expressed in HUVECs and do not influence HUVECs growth. Increased total NOS and eNOS expressions and decreased iNOS expression in HUVECs transfected with Ad-apM1 gene suggest a potential role of Ad-apM1 gene transfer for the prevention and treatment of arteriosclerosis.