• Journal of Chest Surgery
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• v.16 no.4
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• pp.526-532
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• 1983

This is a report of one case of Loffler`s eosinophilic endocarditis associated with mitral insufficiency and LV thrombi treated surgically at the department of Thoracic and Cardiovascular Surgery, Hanyang University Hospital. This patient was a 42 year old female and she has complains of dyspnea, palpitation, orthopnea and generalized edema. Above symptoms has been going for 4 months and NYHA classification was IV. On examination, blood eosinophil was 45 to 50% [WBC-9800 ]. MI and LV thrombi were confirmed by LV ventriculography and echocardiography. Pulmonary congestion and congestive cardiac failure were diagnosis by X-Ray examination, EKG finding and clinical feature and others there were no organic functional disturbance. Mitral valve replacement was performed with Ionescu-Shiley pericardial valve [29mm] replacement. Adjust thumb sized grayish brown colored two thrombi were excluded, lodged in the apex and septal endocardium of LV. Endocardial fibrosis was reliably confirmed under the gross pathology in the heart. The patient had smooth postoperative course and there were no operative complication.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.3
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• pp.259-259
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• 2021

• IMMUNE NETWORK
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• v.16 no.1
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• pp.26-32
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• 2016

Aortic valve stenosis is a heart disease prevalent in the elderly characterized by valvular calcification, fibrosis, and inflammation, but its exact pathogenesis remains unclear. Previously, aortic valve stenosis was thought to be caused by chronic passive and degenerative changes associated with aging. However, recent studies have demonstrated that atherosclerotic processes and inflammation can induce valvular calcification and bone deposition, leading to valvular stenosis. In particular, the most abundant cell type in cardiac valves, valvular interstitial cells, can differentiate into myofibroblasts and osteoblast-like cells, leading to valvular calcification and stenosis. Differentiation of valvular interstitial cells can be trigged by inflammatory stimuli from several immune cell types, including macrophages, dendritic cells, T cells, B cells, and mast cells. This review indicates that crosstalk between immune cells and valvular interstitial cells plays an important role in the development of aortic valve stenosis.

• Journal of Haehwa Medicine
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• v.29 no.1
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• pp.1-17
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• 2020

Objectives : The objectives of this study is to develop a mouse model similar to Taeeum-type by inducing Lung fibrosis with bleomycin, and to determine adequate concentration of bleomycin. Methods : The subjects were divided into six groups: normal, obesity induced group, and bleomycin administered 0.015U, 0.03U, 0.06U, and 0.09U(U/100g bw) concentrations respectively. Each concentration of bleomycin was dissolved in distilled water, and administered through Intra-Nazal-Trachea injection method. Food intake and body weight were measured at regular time weekly. At the end of the experiment, blood was gathered by cardiac puncture for biochemical examinations, organs were removed for histological examinations, and weigh and mRNA genes was analyzed. Result : Mice administered with bleomycin at 0.015U and 0.03U showed body and fat weight gain, and increased blood total cholesterol, LDL-cholesterol, glucose, and free fatty acid level. Fat related genes also showed higher level than the control group. Obesity was most strongly induced in the mice administered with 0.03U of bleomycin. On the other hand, when bleomycin was administered at concentrations above 0.06U, a model of obesity mouse was not created due to rapid emphysema inflammation and weakness. Conclusions : Mice were most vulnerable to obesity when bleomycin was administered at a concentration of 0.3 to cause liver damage. Bleomycin concentration over 0.06U did not cause obesity-induced mice, due to severe damage in liver.

• Journal of Sasang Constitutional Medicine
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• v.28 no.2
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• pp.147-162
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• 2016

Objectives The objective of this study is to develop a taeeumin animal-experimental model induced lung fibrosis with Bleomycin and evaluate the effect on obesity in this animal-experimental model.Methods The subjects were divided into 3 groups : normal group, high fat diet(HFD) control group, and HFD group administered with bleomycin(n=10 per group). To develop taeeumin animal-experimental model with reduced respiratory metabolism, 8-week-old C57BL/6 mice were administered with 0.03ml solution of bleomycin 1U/ml dissolved in distilled water, intratracheal(IT), once. Then, the HFD control group and the experimental group were fed with high fat diet for 6 weeks. Airway hyperresponsiveness(AHR) to methacholine was measured at the 1st and 3rd week after bleomycin was administered. Food intake and body weight were measured at regular time weekly. After the final experiment, blood was gathered by cardiac puncture for bloodchemical examination and organs(liver, fatty tissue) were remoed, weighted, and mRNA was analyzed.Results and Conclusions Through the experiment, it was found that Bleomycin induced Taeeumin animal-experimental models have leptin resistace. In the experimental group administered with Bleomycin, fatty acid synthesizing gene expression increased and energy metabolizing gene expression decreased. As mRNA expression of adiponectin decreased, it was found that Taeeuim animal-experimental model is susceptible to metabolic syndrome and cardiovascular diseases.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.305-314
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• 2016

Inflammatory and fibrotic responses are accelerated during the reperfusion period, and excessive fibrosis and inflammation contribute to cardiac malfunction. NecroX compounds have been shown to protect the liver and heart from ischemia-reperfusion injury. The aim of this study was to further define the role and mechanism of action of NecroX-5 in regulating inflammation and fibrosis responses in a model of hypoxia/reoxygenation (HR). We utilized HR-treated rat hearts and lipopolysaccharide (LPS)-treated H9C2 culture cells in the presence or absence of NecroX-5 ($10{\mu}mol/L$) treatment as experimental models. Addition of NecroX-5 significantly increased decorin (Dcn) expression levels in HR-treated hearts. In contrast, expression of transforming growth factor beta 1 ($TGF{\beta}1$) and Smad2 phosphorylation (pSmad2) was strongly attenuated in NecroX-5-treated hearts. In addition, significantly increased production of tumor necrosis factor alpha ($TNF{\alpha}$), $TGF{\beta}1$, and pSmad2, and markedly decreased Dcn expression levels, were observed in LPS-stimulated H9C2 cells. Interestingly, NecroX-5 supplementation effectively attenuated the increased expression levels of $TNF{\alpha}$, $TGF{\beta}1$, and pSmad2, as well as the decreased expression of Dcn. Thus, our data demonstrate potential antiinflammatory and anti-fibrotic effects of NecroX-5 against cardiac HR injuries via modulation of the $TNF{\alpha}/Dcn/TGF{\beta}1/Smad2$ pathway.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.755-765
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• 2023

Background: Caveolin-1, the scaffolding protein of cholesterol-rich invaginations, plays an important role in store-operated Ca²⁺ influx and its phosphorylation at Tyr14 (p-caveolin-1) is vital to mobilize protection against myocardial ischemia (MI) injury. SOCE, comprising STIM1, ORAI1 and TRPC1, contributes to intracellular Ca²⁺ ([Ca²⁺]_i) accumulation in cardiomyocytes. The purified extract of steamed Panax ginseng (EPG) attenuated [Ca²⁺]_i overload against MI injury. Thus, the aim of this study was to investigate the possibility of EPG affecting p-caveolin-1 to further mediate SOCE/[Ca²⁺]_i against MI injury in neonatal rat cardiomyocytes and a rat model. Methods: PP2, an inhibitor of p-caveolin-1, was used. Cell viability, [Ca²⁺]_i concentration were analyzed in cardiomyocytes. In rats, myocardial infarct size, pathological damages, apoptosis and cardiac fibrosis were evaluated, p-caveolin-1 and STIM1 were detected by immunofluorescence, and the levels of caveolin-1, STIM1, ORAI1 and TRPC1 were determined by RT-PCR and Western blot. And, release of LDH, cTnI and BNP was measured. Results: EPG, ginsenosides accounting for 57.96%, suppressed release of LDH, cTnI and BNP, and protected cardiomyocytes by inhibiting Ca²⁺ influx. And, EPG significantly relieved myocardial infarct size, cardiac apoptosis, fibrosis, and ultrastructure abnormality. Moreover, EPG negatively regulated SOCE via increasing p-caveolin-1 protein, decreasing ORAI1 mRNA and protein levels of ORAI1, TRPC1 and STIM1. More importantly, inhibition of the p-caveolin-1 significantly suppressed all of the above cardioprotection of EPG. Conclusions: Caveolin-1 phosphorylation is involved in the protective effects of EPG against MI injury via increasing p-caveolin-1 to negatively regulate SOCE/[Ca²⁺]_i.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.297-300
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• 2007

Idiopathic hypereosinophilic syndrome is a rare systemic, leukoproliferative disorder characterized by eosinophilmediated tissue injury causing multiple organ failure, including the heart. Cardiac involvement occurs in more than 75% of patients with hypereosinophilic syndrome. Cardiac manifestations include subendocardial fibrosis, thrombus leading to peripheral emboli, restrictive cardiomyopathy, and valvular dysfunction. It is more common in men than in women (9 : 1), and trends to present between the ages of 20 and 50 years. Presentation in childhood is unusual. We report for the first time a case of a 58-year-old man with idiopathic hypereosinophilic syndrome manifested by prosthetic aortic valve dysfunction that was successfully treated by steroid and hydroxyurea therapy after surgical valvular replacement.

• Clinical and Experimental Pediatrics
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• v.60 no.11
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• pp.365-372
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• 2017

Purpose: The mechanism for the pathogenesis of adriamycin (ADR)-induced cardiomyopathy is not yet known. Different hypotheses include the production of free radicals, an interaction between ADR and nuclear components, and a disruption in cardiac-specific gene expression. Apoptosis has also been proposed as being involved in cardiac dysfunction. The purpose of this study was to determine if apoptosis might play a role in ADR-induced cardiomyopathy. Methods: Male Sprague-Dawley rats were separated into 2 groups: the control group (C group) and the experimental group (ADR 5 mg/wk for 3 weeks through intraperitoneal injections; A group). Echocardiographic images were obtained at week 3. Changes in caspase-3, B-cell leukemia/lymphoma (Bcl)-2, Bcl-2-associated X (Bax), interleukin (IL)-6, tumor necrosis $factor-{\alpha}$, brain natriuretic peptide (BNP), troponin I, collagen 1, and collagen 3 protein expression from the left ventricle tissues of C and A group rats were determined by Western blot. Results: Ascites and heart failure as well as left ventricular hypertrophy were noted in the A group. Ejection fraction and shortening fraction were significantly lower in the A group by echocardiography. The expression of caspase-3, Bax, IL-6, BNP, collagen 1, and collagen 3 were significantly higher in the A group as compared with the C group. Protein expression of Bcl-2 decreased significantly in the A group compared with the C group. Conclusion: ADR induced an upregulation of caspase-3, Bax, IL-6, and collagen, as well as a depression in Bcl-2. Thus, apoptosis and fibrosis may play an important role in ADR-induced cardiomyopathy.

• Molecular & Cellular Toxicology
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• v.4 no.4
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• pp.323-330
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• 2008

Surrogate tissue analysis incorporating -omics technologies has emerged as a potential alternative method for evaluating toxic effect of the tissues which are not accessible for sampling. Among the recent applications, blood including whole blood, peripheral blood lymphocytes and peripheral blood mononuclear cells (PBMCs) was suggested as a suitable surrogate tissue in determining toxicant exposure and effect at the pre- or early clinical stage. In this application, we investigated transcriptomic profiles in astemizole treated Cynomolgus monkey's PBMCs. PBMCs were isolated from 4-6 years old male monkeys at 24 hr after administration45 Helvetica Light (10 mg/kg, 30 mg/kg). Gene expression profiles of astemizole treated monkey's PBMCs were determined using Affymetrix $GeneChip^{(R)}$ Human Genome U133 plus 2.0 arrays. The expression levels of 724 probe sets were significantly altered in PBMCs at 10 or 30 mg/kg after astemizole administration following determination of paired t-test using statistical criteria of ${\geq}$$1.5-fold changes at P<0.05. Gene expression patterns in PBMCs showed a considerable difference between astemizole 10 and 30 mg/kg administration groups in spite of an administration of the same chemical. However, close examination using Ingenuity Pathway Analysis (IPA) software revealed that several gene sets related to cardiotoxicity were deregulated at astemizole 10 and 30 mg/kg administration groups. The deregulation of cardiac hypertrophy related genes such as TXN, GNAQ, and MAP3K5 was observed at 10 mg/kg group. In astemizole 30 mg/kg group, genes involved in cardiotoxicity including cardiac necrosis/cell death, dilation, fibrosis, and hypertrophy were also identified. These results suggest that toxicogenomic approach using PBMCs as surrogate tissues will contribute to assess toxicant exposures and identify biomarkers at the pre-clinical stage.