- Impaired Wound Healing in Diabetes Mellitus.
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Min Jeong Kwon, Jeong Hyun Park
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Korean Diabetes J. 2009;33(2):83-90. Published online April 1, 2009
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DOI: https://doi.org/10.4093/kdj.2009.33.2.83
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- The normal healing of a cutaneous wound is achieved via well-orchestrated integration of complex biological and molecular events of cell migration, proliferation, extracellular matrix deposition and tissue remodeling. Chronic wounds fail to progress through the normal stages of healing, and enter a state of pathologic inflammation. Complicated diabetic patients show delayed wound healing caused by multiple factors including vascular insufficiency, abnormalities of the biochemical environment and hyperglycemia per se. Novel technologies including growth factor therapy, gene therapy, stem cell technologies, synthetic skins and hyperbaric oxygen treatment are under development. In the near future, these therapeutic strategies will be clinically available.
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Citations
Citations to this article as recorded by  - Promotion of wound healing through low-fluence ablative fractional laser treatment in diabetic mice
Han Na Lee, Jung Min Bae, Bon Cheol Leo Goo, Young Min Park
Lasers in Medical Science.2019; 34(2): 421. CrossRef - Ethanol Extracts of Chungkookjang Stimulate the Proliferation and Migration of Human Umbilical Vascular Endothelial Cells
Jae Sung Hwang, Dae Il Sung, Whan Myung Lee, Young Shin Chung, Han Bok Kim
The Korean Journal of Microbiology.2014; 50(3): 223. CrossRef - Comparison of Outcome of Trabeculectomy With Mitomycin C and Ahmed Valve Implantation for Uveitic Glaucoma
Joo Yeon Kim, Hyoung Sub Shim, Hwang Ki Kim, Yong Ho Sohn
Journal of the Korean Ophthalmological Society.2010; 51(4): 575. CrossRef
- Cloning of Novel Epidermal Growth Factor (EGF) Plasmid for Gene Therapy on Diabetic Foot Ulcer.
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Hye Sook Chung, Chang Shin Yoon, Min Jeong Kwon, Mi Kyung Kim, Soon Hee Lee, Kyung Soo Ko, Byung Doo Rhee, Jeong Hyun Park
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Korean Diabetes J. 2008;32(2):131-140. Published online April 1, 2008
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DOI: https://doi.org/10.4093/kdj.2008.32.2.131
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2,024
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- BACKGROUND
Epidermal Growth Factor (EGF) is one of the important growth factors involved in the epithelialization during cutaneous wound healing. Peptide EGF has been used for the treatment of diabetic foot ulcer. But the inferiority of cost-effectiveness and the inconvenience of daily application might have restricted its wide clinical usage. EGF gene therapy could dramatically improve the efficacy and inconvenience through long-term expression and bypassing the EGF degradation by hostile non-specific proteinases expressed in the wound bed. METHODS: EGF DNAs were amplified via PCR. For the more effective secretion from the transfected cell, we inserted furin cleavage site into EGF plasmids. The efficacy of novel plasmid pbeta-EGF was verified by transfection into the various animal cell lines, and the biologic potency of expressed EGF was confirmed via phosphorylation of PI3K and GSK3beta by Western blotting. RESULTS: We tested various kinds of human EGFs. One of the human EGF isoforms, EGF(828) including a membrane-anchoring domain was successfully released as the mature EGF protein in the cell culture media. Also EGF plasmid including furin cleavage site showed more than 2-fold increased EGF expression compared with the sequence without furin cleavage site. CONCLUSION: In conclusion, these findings suggest that mature EGF could be released easily out of cells by modifying EGF DNA sequence. Our novel EGF plasmid DNA could markedly increase the efficiency of non-viral gene therapy for diabetic foot ulcer.
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Citations
Citations to this article as recorded by - Effective healing of diabetic skin wounds by using nonviral gene therapy based on minicircle vascular endothelial growth factor DNA and a cationic dendrimer
Min J. Kwon, Songhie An, Sunghyun Choi, Kihoon Nam, Hye S. Jung, Chang S. Yoon, Jung H. Ko, Hye J. Jun, Tae K. Kim, Soo J. Jung, Jeong H. Park, Yan Lee, Jong‐Sang Park
The Journal of Gene Medicine.2012; 14(4): 272. CrossRef
- The Protective Effect of EGCG on INS-1 Cell in the Oxidative Stress and Mechanism.
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Mi Kyung Kim, Hye Sook Jung, Chang Shin Yoon, Min Jeong Kwon, Kyung Soo Koh, Byung Doo Rhee, Jeong Hyun Park
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Korean Diabetes J. 2008;32(2):121-130. Published online April 1, 2008
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DOI: https://doi.org/10.4093/kdj.2008.32.2.121
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2,297
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- BACKGROUND
Oxidative stress is important in both diabetic complications and the development and the progression of type 2 diabetes via the effects on the pancreatic beta-cells. EGCG (epigallocatechin galleate), a major constituent of green tea, has been known to have beneficial effects on various diseases through the mechanisms of antioxidant and cell signaling modulation. But, very small numbers of studies were published about the direct effects of EGCG on the pancreatic beta cell lines. We performed this study to see the protective effect of EGCG on pancreatic beta cell line under H2O2 and the mechanisms of this phenomenon. METHODS: We used INS-1 cells and hydrogen peroxide as an oxidative stressor. Their viabilities were verified by MTT assay and FACS. The activity of glutathione peroxidase was assessed by total glutathione quantification kit. Western blot and semi-quantitative RT-PCR for the catalase, SOD (superoxide dismutase), PI3K and Akt were performed. Functional status of INS-1 cells was tested by GSIS (glucose stimulated insulin secretion). RESULTS: The biological effects of EGCG were different according to its concentrations. 10 micrometer EGCG effectively protected hydrogen peroxide induced damage in INS-1 cells. The expression and the activity of SOD, catalase and the glutathione peroxidase were significantly increased by EGCG. EGCG significantly increased PI3K and Akt activity and its effect was inhibited partially by wortmannin. GSIS was well preserved by EGCG. CONCLUSION: EGCG in low concentration effectively protected INS-1 cells from the oxidative stress through the activation of both antioxidant systems and anti-apoptosis signaling. Further studies will be necessary for the more detailed mechanisms and the clinical implications.
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Citations
Citations to this article as recorded by - Suppressive Effects of Epigallocatechin Gallate Pretreatment on the Expression of Inflammatory Cytokines in RAW264.7 Cells Activated by Lipopolysaccharide
Eun Ji Seo, Jun Go, Ji Eun Kim, Eun Kyoung Koh, Sung Hwa Song, Ji Eun Sung, Chan Kyu Park, Hyun Ah Lee, Dong Seob Kim, Hong Joo Son, Cung Yeoul Lee, Hee Seob Lee, Dae Youn Hwang
Journal of Life Science.2015; 25(9): 961. CrossRef - The Protective Effects of Chrysanthemum cornarium L. var. spatiosum Extract on HIT-T15 Pancreatic β-Cells against Alloxan-induced Oxidative Stress
In-Hye Kim, Kang-Jin Cho, Jeong-Sook Ko, Jae-Hyun Kim, Ae-Son Om
The Korean Journal of Food And Nutrition.2012; 25(1): 123. CrossRef - Protective Effects of Sasa Borealis Leaves Extract on High Glucose-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells
Ji-Young Hwang, Ji-Sook Han
Journal of the Korean Society of Food Science and Nutrition.2010; 39(12): 1753. CrossRef
- Cytoprotective Effect by Antioxidant Activity of Quercetin in INS-1 Cell Line.
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Min Jeong Kwon, Hye Sook Jung, Mi Kyung Kim, Seong Hoon Kang, Gwang Wook Seo, Jae Kwang Song, Tae Yeon Yoon, Min Kyeong Jeon, Tae Hwan Ha, Chang Shin Yoon, Mi Kyung Kim, Woo Je Lee, Jeong Hyun Noh, Soo Kyung Kwon, Dong Joon Kim, Kyung Soo Koh, Byung Doo Rhee, Kyung Ho Lim, Soon Hee Lee, Jeong Hyun Park
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Korean Diabetes J. 2007;31(5):383-390. Published online September 1, 2007
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DOI: https://doi.org/10.4093/jkda.2007.31.5.383
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2,787
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- BACKGROUND
Oxidative stress is induced under diabetic conditions and causes various forms of tissue damages in the patients with diabetes. Recently, pancreatic beta cells are regarded as a putative target of oxidative stress-induced tissue damage, and this seems to explain in part the progressive deterioration of beta cell function in type 2 diabetes. The aim of this study was to examine the potential of Quercetin (QE) to protect INS-1 cells from the H2O2-induced oxidative stress and the effects of QE on the glucose-stimulated insulin secretion in INS-1 cells. METHODS: To study the cell viability, cells were incubated with H2O2 and/or QE at the various concentrations. To confirm the protective effect by QE in response to H2O2, the levels of antioxidant enzymes were assessed by RT-PCR and Western blot, and glutathione peroxidase activities were quantified by spectrophotometrical method. Glucose-stimulated insulin secretion (GSIS) was measured by ELISA. RESULTS: Cell incubations were performed with 80 microM of H2O2 for 5 hours to induce 40 - 50% of cell death. QE gradually showed protective effect (IC50 = 50 microM) in dose-dependent manner. Superoxide dismutase (SOD) mRNA level in H2O2 + QE group was increased as compared to H2O2 group, but catalase did not changed. And the QE recruited glutathione peroxidase activity against H2O2-induced oxidative injuries in INS-1 cells. CONCLUSION: In conclusion, these findings suggest that QE might have protective effect on beta cells by ameliorating oxidative stress and preserving insulin secretory function.
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Citations
Citations to this article as recorded by - Anti-diabetic effects of Allium tuberosum rottler extracts and lactic acid bacteria fermented extracts in type 2 diabetic mice model
Bae Jin Kim, Seung Kyeung Jo, Yoo Seok Jeong, Hee Kyoung Jung
Korean Journal of Food Preservation.2015; 22(1): 134. CrossRef - Protective Effects of Sasa Borealis Leaves Extract on High Glucose-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells
Ji-Young Hwang, Ji-Sook Han
Journal of the Korean Society of Food Science and Nutrition.2010; 39(12): 1753. CrossRef
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