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Ko J.,Paik Memorial Institute for Clinical Research | Jun H.,Paik Memorial Institute for Clinical Research | Chung H.,Paik Memorial Institute for Clinical Research | Yoon C.,Paik Memorial Institute for Clinical Research | And 6 more authors.
Diabetes and Metabolism Journal | Year: 2011

Background: To accelerate the healing of diabetic wounds, various kinds of growth factors have been employed. It is the short half-life of administered growth factors in hostile wound beds that have limited wide-spread clinical usage. To overcome this limitation, growth factor gene therapy could be an attractive alternative rather than direct application of factors onto the wound beds. We administered two growth factor DNAs, epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) into a cutaneous wound on diabetic mice. We compared the different characteristics of the healing wounds. Methods: Streptozotocin was injected intraperitoneally to induce diabetes into C57BL/6J mice. The ultrasound micro-bubble destruction method with SonoVue as a bubbling agent was used for non-viral gene delivery of EGF828 and VEGF165 DNAs. Each gene was modified for increasing efficacy as FRM-EGF828 or minicircle VEGF165. The degree of neoangiogenesis was assessed using qualitative laser Doppler flowmetry. We compared wound size and histological findings of the skin wounds in each group. Results: In both groups, accelerated wound closure was observed in the mice receiving gene therapy compared with non treated diabetic control mice. Blood flow detected by laser doppler flowmetry was better in the VEGF group than in the EGF group. Wound healing rates and histological findings were more accelerated in the EGF gene therapy group than the VEGF group, but were not statistically significant. Conclusion: Both non-viral EGF and VEGF gene therapy administrations could improve the speed and quality of skin wound healing. However, the detailed histological characteristics of the healing wounds were different. © 2011 Korean Diabetes Association. Source

Kim M.K.,Maryknoll Medical Center | Kim M.K.,Paik Memorial Institute for Clinical Research | Jung H.S.,Paik Memorial Institute for Clinical Research | Yoon C.S.,Paik Memorial Institute for Clinical Research | And 14 more authors.
Frontiers in Bioscience - Elite | Year: 2010

EGCG and quercetin are known as beneficial dietary flavonoid for various diseases including diabetes mellitus. But it is not certain whether they could protect pancreatic beta cell directly. We performed this study to test both EGCG and quercetin could directly protect beta cell line under oxidative stress, and verify the action mechanisms. The protective effect of quercetin on INS-1 cells against oxidative stress was concentration dependent, but EGCG showed specific concentration zone for the protection. The protective effect of EGCG was more pronounced in pre-treatment before oxidative stress, while quercetin showed dramatic improvement of viability in simultaneous incubation with H 2O2. In EGCG pretreatment, antioxidant enzymes and activity were decreased, but the phosphorylated PI3K and Akt were significantly increased. PI3K inhibitor significantly reduced cell viability in EGCG pre-treatment. In conclusion, EGCG and quercetin have protective effect on INS-1 cells against oxidative stress through both antioxidant effect and antiapoptosis signaling. In EGCG, pre-treatment make its effect better by the enhancement of anti-apoptosis signaling. Quercetin protected INS-1 cells more in simultaneous incubation via strong antioxidant defense. 1.AE Butler, J Janson, S Bonner-Weir, R Ritzel, RA Rizza, PC Butler: Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Source

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