• Current Optics and Photonics
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• v.3 no.6
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• pp.485-495
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• 2019

Photobiomodulation (PBM) using organic light emitting diodes (OLEDs) surface light sources have recently been claimed to be the next generation of PBM light sources. However, the differences between light emitting diodes (LEDs) and OLED mechanisms in vitro and in vivo have not been well studied. In vivo mouse models were used to investigate the effects of OLED irradiation on cellular function and cutaneous wound healing compared to LED irradiation. Mice in the LED- and OLED-irradiated groups were subjected to irradiation with 6 J/㎠ LED and OLED (630 nm), respectively, for 14 days after wounding, and some mice were sacrificed for the experiments on days 3, 7, 10, and 14. To evaluate wound healing, we performed hematoxylin-eosin and Masson's trichrome staining and quantified collagen density by computerized image analysis. The results showed that the size of the wound, collagen density, neo-epidermis thickness, number of new blood vessels, and number of fibroblasts and neutrophils was significantly influenced by LED and OLED irradiation. The tissue levels of interleukin (IL)-β, IL-6 and tumor necrosis factor (TNF)-α were investigated by immunohistochemical staining. LED and OLED irradiation resulted in a significant increase in the tissue IL-β and IL-6 levels at the early stage of wound healing (P < 0.01), and a decrease in the tissue TNF-α level at all stages of wound healing (P < 0.05), compared to the no-treatment group. The expression levels of the genes encoding vascular endothelial growth factor and transforming growth factor-beta 1 were significantly increased in LED and OLED-irradiated wound tissue at the early stage of wound healing (P < 0.01) compared to the no-treatment group. Thus, OLED as well as LED irradiation accelerated wound healing by modulating the synthesis of anti-inflammatory cytokines and the expression levels of genes encoding growth factors, promoting collagen regeneration and reducing scarring. In conclusion, this suggests the possibility of OLED as a new light source to overcome the limitations of existing PBMs.

• The Journal of Advanced Prosthodontics
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• v.2 no.1
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• pp.7-13
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• 2010

Although most researchers agree that platelet-rich plasma (PRP) is a good source of autogenous growth factors, its effect on bone regeneration is still controversial. The purpose of this study was to evaluate whether increasing angiogenic factors in the human PRP to enhance new bone formation through rapid angiogenesis. MATERIAL AND METHODS. In vitro, the human platelets were activated with application of shear stress, $20\;{\mu}g/ml$ collagen, 2 mM $CaCl_2$ and 10U thrombin/$1\;{\times}\;10^9$ platelets. Level of vascular endothelial growth factor (VEGF) and platelet microparticle (PMP) in the activated platelets were checked. In the animal study, human angiogenic factors-enriched PRP was tested in 28 athymic rat's cranial critical bone defects with $\beta$-TCP. Angiogenesis and osteogenesis were evaluated by laser Doppler perfusion imaging, histology, dual energy X-ray densinometry, and micro-computed tomography. RESULTS. In vitro, this human angiogenic factors-enriched PRP resulted in better cellular proliferation and osteogenic differentiation. In vivo, increasing angiogenic potential of the PRP showed significantly higher blood perfusion around the defect and enhanced new bone formation around acellular bone graft material. CONCLUSION. Angiogenic factor-enriched PRP leads to faster and more extensive new bone formation in the critical size bone defect. The results implicate that rapid angiogenesis in the initial healing period by PRP could be supposed as a way to overcome short term effect of the rapid angiogenesis.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.4
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• pp.323-328
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• 2017

Angiogenesis is a process including members of the angiogenic factors. In particular, fibroblast growth factor 2 (FGF2) is considered the most potent angiogenic factor because it promotes cell proliferation and tube formation. A recent study reported that fucoidan derived from marine plant potentiated FGF-2 induced tube formation in human endothelial cells. On the other hand, the molecular mechanisms involved in the angiogenic activity of fucoidan and FGF2 are unknown. In this study, a fucoidan treatment promoted angiogenesis induced by FGF2. The effects of fucoidan on FGF2-induced angiogenesis were confirmed by a proliferation assay using a CellTiter96 Aqueous One solution after a treatment with fucoidan and FGF2. The tube formation and wound healing assay for the angiogenic activity were also confirmed. Reverse transcription PCR showed a change in the mRNA of vascular endothelial growth factor-A (VEGF-A), intercellular adhesion molecule-1 (ICAM-1), matrix metallopeptidase9 (MMP9), and the signal transducer and activator of transcription3 (STAT3). In summary, the Fucoidan/FGF2 treatment induced an increase in cell proliferation, improved the tube formation and wound healing activity, and altered the STAT3, VEGF-A, ICAM-1, and MMP9 mRNA expression levels. Further research will be needed to provide a scientific explanation in terms of cell-signaling and confirm the present findings.

• Clinical and Experimental Pediatrics
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• v.46 no.8
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• pp.811-816
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• 2003

Purpose : Kawasaki disease is an acute systemic vasculitis of unknown etiology with a predilection for the coronary arteries. Vascular endothelial growth factor(VEGF) is a cytokine which promotes vascular permeability and angiogenesis. We investigated serum VEGF(sVEGF) levels in Kawasaki disease to determine whether sVEGF level can be used as a risk factor to predict the occurrence of coronary artery lesions(CAL) in Kawasaki disease. Methods : We measured sVEGF levels in 11 patients with Kawasaki disease in acute phase(patient group)and 11 normal children(control group) by enzyme-linked immunosorbent assay(ELISA) method. We investigated the relationship between sVEGF levels and the lumen diameters of coronary artery and other potential CAL risk factors; duration of fever, hemoglobin, WBC counts, platelet counts, ESR, CRP and LDH levels. Results : SVEGF levels of patients in the acute phase of Kawasaki disease(mean $847.9{\pm}495.7pg/mL$) were significantly higher than that of normal controls(mean $279.9{\pm}150.6pg/mL$; P<0.05). SVEGF levels showed significant positive correlation with the lumen diameters of the coronary artery(P<0.05, $r_s=0.75$) in the patient group. There was no significant correlation between sVEGF levels and duration of fever or other laboratory measurements. Conclusion : Our results support the notion that sVEGF level may be considered as a predictive indicator for the occurrence of coronary artery lesions in Kawasaki disease.

• Journal of Society of Preventive Korean Medicine
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• v.16 no.1
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• pp.57-70
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• 2012

The apoptotic process of gastric mucosa triggered by induction of proapoptotic gene expression, such as Bax. Stress-inducing factors may affect Bcl-2/Bax ratio and thus the rate of apoptosis through modulation of the expression of both proteins depending upon the experimental model. TGF-${\beta}$ is believed to be essential in wound healing for regulation of cell growth and differentiation and is known to be involved in tissue repair and remodeling. The polypeptide growth factors, such as vascular endothelial growth factor(VEGF), regulate essential cell functions involved in tissue healing including cell proliferation, migration, and differentiation. The purpose of this study was to investigate whether the oral administration of $Hwangyeon-tang$ (HYT) would have protect effects on gastric ulcer in rat. Sprague-Dawley rats (n=40) were randomly divided into 4 groups ; Normal, Saline, Cimetidine and HYT group. The saline, cimetidine and HYT extract were orally administrated to each group and gastric ulcer was induced with HCl/EtOH solution. After 1 hour, the stomachs were collected for histological observation and immunohistochemistry. In Results, the wound healing of gastric ulcer was promoted by HYT and the significant alterations of BAX/Bcl-2, TGF-${\beta}1$ and VEGF proteins in gastric mucosa were observed. These results suggest that Fritillaria ussuriensis extract promotes wound healing and has protective effects on gastric ulcer in rats.

• Journal of Society of Preventive Korean Medicine
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• v.14 no.1
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• pp.97-110
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• 2010

The wound healing process can be categorized as follows : inflammation, fibroplasia, neovascularization, collagen deposition, epithelialization, and wound contraction. During the healing process, various growth factors are secreted to accelerate wound healing. Previous studies have demonstrated that endogenous growth factors, such as vascular endothelial growth factor(VEGF) are the important regulatory polypeptides for coordinating the healing process. They are released from macrophages, fibroblasts, and keratinocytes at the site of injury and participate in the regulation of reepithelization, granulation tissue formation, collagen synthesis and neovascularization. Onchung-Um has been used clinically to treat various skin diseases. In addition, Onchung-Um has been also used for congestive inflammations. In the present study, we evaluated the effects of Onchung-Um on wound healing process and wound size reduction in rats. Full-thickness skin wounds ($15mm\;{\times}\;15mm$) were created on the back of rats. Rats were then divided into 2 groups : The Onchung-Um treated group that was orally administered with a dose of 193.9mg/100g of Onchung-Um extract per day for 15 days and Control group without Onchung-Um administration. Moreover, the histological changes and VEGF immunoexpressions of two groups were estimated. In results, wound closures were significantly accelerated by oral administration of Onchung-Um extract. Furthermore, in Onchung-Um treated group, there were significant increases in fibroblast migration, epithelialization compared with the Control group. VEGF expressions were also increased in Onchung-Um treated group. This study has therefore demonstrated the Onchung-Um can significantly improve the quality of wound healing and scar formation and the oral administration of Onchung-Um extract may increase early tissue angiogenesis in the incisional wound of an experimental animal model.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.1
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• pp.71-77
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• 2011

Gastric ulcer has multifactorial etiology, and the development of ulcer is known to be caused by gastric acidity, pepsin secretion, gastric motility and gastric mucosal blood flow. The ulcer results from the tissue necrosis and apoptotic cell death triggered by mucosal ischemia, free radical formation and cessation of nutrient delivery. The gastric mucosa is usually exposed to a wide range of aggressive insults, and has developed efficient mechanisms to repair tissue injury. The apoptotic process of gastric mucosa is triggered by the induction of such proapoptotic gene expression, such as BAX. The Bcl-2 family of proteins plays a pivotal role in the regulation of apoptosis. The maintenance of gastric mucosa integrity depends upon the ratio between cell proliferation and cell death. Stress-inducing factors may affect Bcl-2/BAX ratio and thus the rate of apoptosis through modulation of the expression of both proteins depends upon the experimental model. In addition to the regulation of apoptosis, new vessels have to be generated in order to ensure an adequate supply of oxygen and nutrients to the healing gastric mucosa. This events are regulated by several factors. Among them, such polypeptide growth factors, such as vascular endothelial growth factor (VEGF) regulates essential cell functions involved in tissue healing including cell proliferation and differentiation. The purpose of this study was carried to investigate whether Rhei Rhizoma administration might protect apoptotic cell death and promote angiogenesis in gastric mucosa. Sprague-Dawley rats were randomly divided into 4 groups; normal, saline, cimetidine and Rhei Rhizoma-treated group. The saline, cimetidine and Rhei Rhizoma extracts were orally administrated to each group and gastric ulcer was induced by HCl-EtOH solution. After 1 hour, the stomachs were collected for histological observation and immunohistochemistry. In results, Rhei Rhizoma proves to promote to heal wound in gastric ulcer in conclusion and the significant changes of BAX, Bcl-2 and VEGF quantity in gastric mucosa were observed. These results suggest that Rhei Rhizoma extract may promote incision wound healing and has protective effects on gastric ulcer in rats.

• Journal of Korean Neurosurgical Society
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• v.62 no.2
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• pp.153-165
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• 2019

Objective : Spinal cord injury (SCI) is a very serious health problem, usually caused by a trauma and accompanied by elevated levels of inflammation indicators. Stem cell-based therapy is promising some valuable strategies for its functional recovery. Nestin-positive progenitor and/or stem cells (SC) isolated from pancreatic islets (PI) show mesenchymal stem cell (MSC) characteristics. For this reason, we aimed to analyze the effects of rat pancreatic islet derived stem cell (rPI-SC) delivery on functional recovery, as well as the levels of inflammation factors following SCI. Methods : rPI-SCs were isolated, cultured and their MSC characteristics were determined through flow cytometry and immunofluorescence analysis. The experimental rat population was divided into three groups : 1) laminectomy & trauma, 2) laminectomy & trauma & phosphate-buffered saline (PBS), and 3) laminectomy+trauma+SCs. Green fluorescent protein (GFP) labelled rPI-SCs were transplanted into the injured rat spinal cord. Their motilities were evaluated with Basso, Beattie and Bresnahan (BBB) Score. After 4-weeks, spinal cord sections were analyzed for GFP labeled SCs and stained for vimentin, $S100{\beta}$, brain derived neurotrophic factor (BDNF), 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase), vascular endothelial growth factor (VEGF) and proinflammatory (interleukin [IL]-6, transforming growth factor $[TGF]-{\beta}$, macrophage inflammatory protein [MIP]-2, myeloperoxidase [MPO]) and anti-inflammatory (IL-1 receptor antagonis) factors. Results : rPI-SCs were revealed to display MSC characteristics and express neural and glial cell markers including BDNF, glial fibrillary acidic protein (GFAP), fibronectin, microtubule associated protein-2a,b (MAP2a,b), ${\beta}3$-tubulin and nestin as well as anti-inflammatory prostaglandin E2 receptor, EP3. The BBB scores showed significant motor recovery in group 3. GFP-labelled cells were localized on the injury site. In addition, decreased proinflammatory factor levels and increased intensity of anti-inflammatory factors were determined. Conclusion : Transplantation of PI-SCs might be an effective strategy to improve functional recovery following spinal cord trauma.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.3
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• pp.2053-2058
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• 2013

Background: Formation of new blood vessels is necessary for the development and spread of neoplasms more than 1 mm3 in volume, angiogenesis being responsible for formation of new from pre-existing blood vessels. Vascular endothelial growth factor (VEGF) is pivotal and the best studied angiogenic factor in all human cancers. Therefore we designed this study to investigate the role of VEGF-A and VEGF-C in prostate cancer in comparison with BPH controls in a north Indian population. Methods: In this case-control study a total of 100 subjects were included on the basis of confirmed histopathological reports, out of which 50 were prostate cancer patients and the other 50 were BPH patients with PSA levels >2 ng/ml and abnormal digital rectal examination (DRE) findings during September 2009 to August 2011 from the Department of Urology, KGMU, Lucknow, India. Plasma levels of VEGF were determined using quantitative immunoassay (ELISA-enzyme linked immunosorbent assay). Statistical analysis was carried out using SPSS 15.0 version. Results: The mean age of prostate cancer ($67.6{\pm}5.72$) patients was significantly higher (p=0.005) than BPH ($63.6{\pm}7.92$) patients. Expression of VEGF-A was not significantly higher in disease stage C1 than D1 or D2 and A or B (p=0.13) while the level of VEGF-A was significantly higher (p=0.04) in prostate cancer as compared to BPH subjects (PCa=13.0 pg/ml, BPH=6.8 pg/ml). Levels of VEGF-C were similar in both groups (PCa=832.6 pg/ml, BPH=823.7 pg/ml). In ROC curve, the area under curve (AUC) was 0.70 (95%CI: 0.60-0.80) and the cut-off value for which a higher proportion of patients was correctly classified (20%) was 26.0 pg/mL. Conclusion: Although VEGF-A is increased in cancer prostate patients a statistically significant correlation could not be established in this study. VEGF-C was not found to be a useful biomarker.

• Clinical and Experimental Pediatrics
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• v.50 no.12
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• pp.1241-1246
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• 2007

Purpose : Recently, there has been several studies to clarify the pathogenesis of Kawasaki disease (KD) and the relations of VEGF and endostatin that act on vascular endothelial cells to the coronary artery complications. In this report, we measured serum levels of VEGF and endostatin in acute and subacute phases of KD to assess the change of these levels and the relations to the development of coronary artery lesions (CAL). Methods : Twenty six patients were diagnosed and treated for KD between January, 2001 and July, 2005 at Kangnam St. Mary's Hospital, the Catholic University of Korea. They were divided into those with and without CAL. Serum levels of VEGF and endostatin were measured during acute and subacute phases and compared to those measured in healthy and disease control groups. Results : Serum levels of VEGF were increased in KD but no differences were noted in KD with and without CAL. Serum levels of endostatin were decreased in the acute phase of KD, however they were recovered in the subacute phase of KD, regardless of CAL. The VEGF/endostatin ratio was increased in KD. KD without CAL showed a relative decrease in this ratio during the subacute phase. Significant positive correlations were found between serum VEGF and WBC count, VEGF and ESR, VEGF/endostatin ratio and ESR in the acute phase of KD. Conclusion : Analysis of factors influencing the vascular endothelium such as VEGF and endostatin will help to clarify the etiology of KD and the pathogenesis of CAL.