• Journal of Physiology & Pathology in Korean Medicine
• /
• v.20 no.6
• /
• pp.1567-1571
• /
• 2006

Lophatheri Herba of Lophatherum gracile Bronghiart(Gramineae) has long been used for treatment of inflammation, fever and edema in Korea. In order to investigate antibacterial activity of the Lophatheri Herba against Streptococcus mutans ATCC27351, paper disc test and pH check were carried out with 80% ethanol extract of Lophatheri Herba(LEX). The LEX showed significant antibacterial activity. And at the dose of 50 mg/kg, LEX showed signifiant inhibition on the paw edema, vascular permeability and myeloperoxidase activity in rat's paw tissue. These results indicate that LEX has antibacterial activity against the Streptococcus mutans and anti-inflammatory effect.

• Biomedical Science Letters
• /
• v.25 no.1
• /
• pp.66-74
• /
• 2019

Hyperlipidemia is defined as conditions of the accumulation of lipids such as free fatty acids (FFA), triglyceride (TG), cholesterol and/or phospholipid in the bloodstream. Hyperlipidemia can cause lipid accumulation in non-adipose tissue, which is lipid-cytotoxic effects in many tissues and mediates cell dysfunction, inflammation or programmed cell death (PCD). TG is considered to be a major cause of atherosclerosis through inflammatory necrosis of vascular endothelial cells. Recently, TG have also been shown to exhibit lipid-cytotoxicity and induce PCD. Therefore, we investigated the effect of TG on the cytotoxic effect of various cell types. When exposed to TG, the cell viability of U937 monocytes and Jurkat T lymphocytes, as well as the cell viability of MCF-7, a non-immune cell, decreased in time- and dose-dependent manner. In U937 cells and Jurkat cells, caspase-9, an intrinsic apoptotic caspase, and caspase-8, an extrinsic apoptotic caspase, were increased by exposure to TG. However, in TG-treated MCF-7 cells, caspase-8 activity increased only without caspase-9 activity. In addition, the reduction of cell viability by TG was recovered when all three cell lines were treated with pan-caspase inhibitor. These results suggest that activation of apoptotic caspases by TG causes lipotoxic effect and decreases cell viability.

• Archives of Plastic Surgery
• /
• v.48 no.4
• /
• pp.448-456
• /
• 2021

Background Locoregional stem cell delivery is very important for increasing the efficiency of cell therapy. Amnisite BA (Amnisite) is a freeze-dried amniotic membrane harvested from bovine placenta. The objective of this study was to investigate the retention of cells of the stromal vascular fraction (SVF) on Amnisite and to determine the effects of cell-loaded Amnisite in a porcine radiation-induced chronic wound model. Methods Initially, experiments were conducted to find the most suitable hydration and incubation conditions for the attachment of SVF cells extracted from pig fat to Amnisite. Before seeding, SVFs were labeled with PKH67. The SVF cell-loaded Amnisite (group S), Amnisite only (group A), and polyurethane foam (group C) were applied to treat radiation-induced chronic wounds in a porcine model. Biopsy was performed at 10, 14, and 21 days post-operation for histological analysis. Results Retaining the SVF on Amnisite required 30 minutes for hydration and 1 hour for incubation. A PKH67 fluorescence study showed that Amnisite successfully delivered the SVF to the wounds. In histological analysis, group S showed increased re-epithelialization and revascularization with decreased inflammation at 10 days post-operation. Conclusions SVFs had acceptable adherence on hydrated Amnisite, with successful cell delivery to a radiation-induced chronic wound model.

• Journal of Yeungnam Medical Science
• /
• v.40 no.4
• /
• pp.328-334
• /
• 2023

An aging population and changes in dietary habits have increased the incidence of diabetes, resulting in complications such as diabetic foot ulcers (DFUs). DFUs can lead to serious disabilities, substantial reductions in patient quality of life, and high financial costs for society. By understanding the etiology and pathophysiology of DFUs, their occurrence can be prevented and managed more effectively. The pathophysiology of DFUs involves metabolic dysfunction, diabetic immunopathy, diabetic neuropathy, and angiopathy. The processes by which hyperglycemia causes peripheral nerve damage are related to adenosine triphosphate deficiency, the polyol pathway, oxidative stress, protein kinase C activity, and proinflammatory processes. In the context of hyperglycemia, the suppression of endothelial nitric oxide production leads to microcirculation atherosclerosis, heightened inflammation, and abnormal intimal growth. Diabetic neuropathy involves sensory, motor, and autonomic neuropathies. The interaction between these neuropathies forms a callus that leads to subcutaneous hemorrhage and skin ulcers. Hyperglycemia causes peripheral vascular changes that result in endothelial cell dysfunction and decreased vasodilator secretion, leading to ischemia. The interplay among these four preceding pathophysiological factors fosters the development and progression of infections in individuals with diabetes. Charcot neuroarthropathy is a chronic and progressive degenerative arthropathy characterized by heightened blood flow, increased calcium dissolution, and repeated minor trauma to insensate joints. Directly and comprehensively addressing the pathogenesis of DFUs could pave the way for the development of innovative treatment approaches with the potential to avoid the most serious complications, including major amputations.

• Annals of Hepato-Biliary-Pancreatic Surgery
• /
• v.26 no.2
• /
• pp.204-209
• /
• 2022

The state of intense peripancreatic inflammation in chronic pancreatitis can give rise to various vascular complications such as venous thrombosis and arterial pseudoaneurysms. Due to its intimate location with the pancreas, spleno-mesenteric-portal axis suffers the greatest blunt of thrombotic complications. Treatment modalities for such cases of chronic portal vein thrombosis have always been controversial and challenging. Medical management with anticoagulants is both risky and unsatisfactory due to presence of varices, hypersplenism, and persistence of the inflammatory pathology. Although endovascular techniques have been tried in various case reports, there are definite anatomical challenges in cases of long segment porto-mesenteric thrombosis with massive ascites. Surgical shunts have been historically described for cirrhotic and non-cirrhotic portal hypertensive patients. However, its use in patients with refractory ascites due to chronic pancreatitis induced portal vein thrombosis has not been reported in the medical literature. Here, we present a case of an extensive portal vein thrombosis with massive refractory ascites in a patient with alcohol-induced chronic pancreatitis successfully treated with a surgical mesocaval shunt using an interposition small diameter graft.

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.4
• /
• pp.377-384
• /
• 2017

Activation of protein kinase C (PKC) is closely linked with endothelial dysfunction. However, the effect of $PKC{\beta}II$ on endothelial dysfunction has not been characterized in cultured endothelial cells. Here, using adenoviral $PKC{\beta}II$ gene transfer and pharmacological inhibitors, the role of $PKC{\beta}II$ on endothelial dysfucntion was investigated in cultured endothelial cells. Phorbol 12-myristate 13-acetate (PMA) increased reactive oxygen species (ROS), p66shc phosphorylation, intracellular adhesion molecule-1, and monocyte adhesion, which were inhibited by $PKC{\beta}i$ (10 nM), a selective inhibitor of $PKC{\beta}II$. PMA increased the phosphorylation of CREB and manganese superoxide dismutase (MnSOD), which were also inhibited by $PKC{\beta}i$. Gene silencing of CREB inhibited PMA-induced MnSOD expression, suggesting that CREB plays a key role in MnSOD expression. Gene silencing of $PKC{\beta}II$ inhibited PMA-induced mitochondrial ROS, MnSOD, and ICAM-1 expression. In contrast, overexpression of $PKC{\beta}II$ using adenoviral $PKC{\beta}II$ increased mitochondrial ROS, MnSOD, ICAM-1, and p66shc phosphorylation in cultured endothelial cells. Finally, $PKC{\beta}II$-induced ICAM-1 expression was inhibited by Mito-TEMPO, a mitochondrial ROS scavenger, suggesting the involvement of mitochondrial ROS in PKC-induced vascular inflammation. Taken together, the results suggest that $PKC{\beta}II$ plays an important role in PMA-induced endothelial dysfunction, and that the inhibition of $PKC{\beta}II$-dependent p66shc signaling acts as a therapeutic target for vascular inflammatory diseases.

• Journal of Embryo Transfer
• /
• v.33 no.3
• /
• pp.129-137
• /
• 2018

Acute vascular rejection has been known as a main barrier occurring in a xenograted tissue of alpha 1,3-galactosyltransferase knock-out (GalT KO) pig into a non-human primate (NHP). Adenosine which is a final metabolite following sequential hydrolysis of nucleotide by ecto-nucleotidases such as CD39 and CD73, act as a regulator of coagulation, and inflammation. Thus xenotransplantation of CD39 and CD73 expressing pig under the GalT KO background could lead to enhanced survival of recipient NHP. We constructed a human CD39 and CD73 expression cassette designed for endothelial cell-specific expression using porcine Icam2 promoter (pIcam2-hCD39/hCD73). We performed isolation of endothelial cells (pAEC) from aorta of 4 week-old GalT KO and membrane cofactor protein expressing pig ($GalT^{-MCP/-MCP}$). We were able to verify that isolated cells were endothelial-like cells using immunofluorescence staining analysis with von Willebrand factor antibody, which is well known as an endothelial maker, and tubal formation assay. To find optimal condition for efficient transfection into pAEC, we performed transfection with GFP expression vector using four programs of nucleofection, M-003, U-023, W-023 and Y-022. We were able find that the program W-023 was optimal for pAEC with regard to viability and transfection efficiency by flow cytometry and fluorescent microscopy analyses. Finally, we were able to obtain $GalT^{-MCP/-MCP}/CD39/CD73$ pAEC expressing CD39 and CD73 at levels of 33.3% and 26.8%, respectively. We suggested that pACE isolated from $GalT^{-MCP/-MCP}$ pig might be provided as a basic resource to understand biochemical and molecular mechanisms of the rejections and as an alternative donor cells to generate $GalT^{-MCP/-MCP}/CD39/CD73$ pig expressing CD39 and CD73 at endothelial cells.

• The Journal of Korean Medicine
• /
• v.26 no.2 s.62
• /
• pp.77-84
• /
• 2005

Objectives: Chunghyul-dan is a combinatorial herbal medicine, and previous studies reported it had therapeutic effects for microangiopathy, which is a major part. in the progression of stroke, as well as having anti-hypertensive, anti-hyperlipidemic, anti-apoptotic, anti-oxidative, and anti-inflammatory activities, Therefore, we examined the inhibitory effect of Chunghyul-dan on stroke occurrence in patients with silent brain infarction. Methods: We prescribed Chunghyul-dan at 600 mg a day to patients with silent brain infarction confirmed by brain MRI, and monitored stroke occurrence, drug compliances, and adverse effects for 1 year, We then performed follow-up brain MRI to detect new vascular lesions after 1 year of Chunghyul-dan medication. As for the subjects lost to follow-up, we assessed their prognosis after 1 year by telephone. Results: There were twenty-one subjects who were treated with Chunghyul-dan for more than 1 year, None of them experienced new clinical syndromes characterized by rapidly developing clinical symptoms and signs of focal and at times global loss of brain function, which could be accompanied with evidence of stroke occurrence, or any adverse effects during the Chunghyul-dan medication period. These results might be explained by various biochemical effects of Chunghyul-dan on microangiopathy, which is closely related with cell cycle progression, hypertension, hyperlipidemia, vascular inflammation, and oxidative damage. Of the 10 subjects lost to follow-up, six were reached; two of them had stroke occurrence. Conclusions: We suggest Chunghyul-dan could be useful for prevention of stroke occurrence in patients with silent brain infarction by preventing the progression of microangiopathy. Further study with a randomized controlled trial is needed to confirm this suggestion.

• Korean Journal of Head & Neck Oncology
• /
• v.17 no.2
• /
• pp.155-161
• /
• 2001

Background and Objectives: Nitric oxide (NO) is generated in mammalian tissue by the conversion of L-arginine to L-citrulline. This reaction is catalyzed by nitric oxide synthase (NOS). NO is an important bioactive agent and a signalling molecule that mediates a variety of biologic actions such as vasodilation, neurotransmission, host defense, and iron metabolism but increased NO production may also contribute to the pathogenesis of a various of disorders, including cancer. Before now, the role of NO in thyroid gland is still investigated and it was supposed that NO mediate the angiogenesis in tumor growth. Others journal and works identified the expression of iNOS that involve by neutrophil and eNOS that involve in part in the vascular remodeling and to understand the role of NO in human thyroid gland. But authors revealed only eNOS in thyroid neoplasm. iNOS was identifed by inflammation in fault. Materials and Methods: Western blot analysis was performed, using a polyclonal antibody against eNOS (Rabbit polyclonal IgG). Using the same antibody, the distribution of eNOS was examined in 15 formalin-fixed paraffin embedded samples by immunohistochemistry. By NADPH consumption rate, NOS activity was estimated at nodular hyperplasia. Results: Western blot analysis exhibited that eNOS was significantly elevated in thyroid papillary carcinoma, compared to that in nodular hyperplasia and normal tissue. Immunohistochemistry showed that the immunoreacitivity was present more significantly in thyroid follicular epithelial cell layer than vascular endothelial cell. NOS activity increased in nodular hyperplasia. Conclusions: Thyroid papillary cancer without neutrophil invasion expressed only eNOS. The endothelial localization of eNOS may play an important role in pathogenensis of human thyroid nodular hyperplasia and the follicular localization of thyroid papillary carcinomas.

• Clinical and Experimental Pediatrics
• /
• v.53 no.1
• /
• pp.41-47
• /
• 2010

Purpose : Adiponectin is an endogenous modulator of vascular remodeling that suppresses vascular inflammation. However, the role of adiponectin in Kawasaki disease (KD) has not been elucidated. The purpose of this study is to investigate the correlation between serum adiponectin level and several parameters, such as interleukin (IL)-6, tumor necrosis factor $(TNF)-{\alpha}$, lipid profile, and C reactive protein (CRP), and to clarify the association between adiponectin and cardiac function. Methods : Twenty-two KD patients (22 patients in acute phase and 20 patients in subacute phase) were enrolled in the study group. The control group consisted of 31 subjects (13 febrile patients and 18 healthy children). Both groups underwent blood sampling and tissue Doppler imaging (TDI). Results : CRP was significantly increased in the KD group compared with the control group. There were no significant differences in serum $TNF-{\alpha}$, IL-6, and adiponectin levels between groups. However, a negative correlation was found between adiponectin level and CRP level or platelet count. Systolic myocardial velocity and A myocardial velocity measured by TDI were decreased significantly in the acute KD group compared with the subacute KD group and control group. Positive correlations were found between adiponectin level and systolic myocardial velocity or A myocardial velocity. Conclusion : In acute KD patients, low adiponectin level was related to severe inflammatory reactions and decreased left ventricular functions.