• Proceedings of the PSK Conference
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• 2003.10b
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• pp.86.2-87
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• 2003

Introduction: Liver fibrosis is defined unbalance of collagen metabolism, especially a stimulation of collagen synthesis and inhibition of collagen degradation, and antifibrotic effect is delaying or inhibition of new collagen synthesis and deposition in liver tissue. In this study, we investigated the antifibrotic and antioxidative effect of Solanum lycopersicum (SL) in liver fibrosis induced rats. Methods: : Rats were randomly divided in three groups (normal, CCl$_4$ and CCl$_4$-SL group) and were received 0.6 ml mixture of CCl$_4$ and olived oil (1:1 v/v) 3 times/week for 4 weeks except of the normal group. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.176.1-176.1
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• 2003

The protective effects on hepatic fibrosis of an aqueous extract from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil (CK), in hepatic stellate cell line, CFSC-2G. The increased deposition of extracellular matrix by hepatic stellate cells following liver injury in a process known as activation is considered a key mechanism for increased collagen content of liver during the development of liver fibrosis. (omitted)

• Laboraroty Animal Research
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• v.33 no.2
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• pp.76-83
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• 2017

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of $Pycnogenol^{(R)}$ (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in $TGF-{\beta}1$/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

• YAKHAK HOEJI
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• v.51 no.1
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• pp.7-12
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• 2007

Hepatic cirrhosis is an important feature of chronic liver disease. Liver cirrhosis is characterized by hyperaccumulation of fibrous tissue components and is commonly observed in latter or terminal states of chronic hepatic disease. The antifibrotic effects on liver cirrhosis by oriental herbs extraction material were examined in bile duct ligated rats. Oriental herbs extraction (0.99 mg/kg rat weight/day) was administrated to cirrohotic rats for 4 weeks. Liver collagen content of bile duct ligated rats was significantly increased. And liver histology showed collagen fiber deposition was increased as well as the normal architecture was lost with large zone of necrosis being observed. Herbs extraction administrated rats showed significantly decreased liver collagen content, accumulation of collagen fiber in histological analysis, and biochemical markers of hepatic diseases. Those results demonstrate the usefulness of herbs extraction materials as an antifibrotic agent for liver cirrhosis.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.18 no.3
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• pp.488-499
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• 1996

Diabetes mellitus revealed a chronic disorder of lipid, carbohydrate and protein metabolism characterized by insulin deficiency, and a striking tendency toward development of atherosclerosis, microangiopathy, nephropathy, neuropathy and recently cardiomyopathy etc. The mechanism of heart failure in patients with diabetic cardiomyopathy is not clear but diabetic cardiomyopathy usually occurs in persons with long standing diabetes. After diabetes induced in made Sprague- Dawley strain rats by injection of streptozotocin(60mg/kg), cardiac tissue with hematoxylin-eosin and Masson's trichrome stain was examined at 3 days, 1, 2, 4, 6 weeks later under light microscope. The results were obtained as follows : 1. In H&E stain of control group, myocardiac cells were shorter than skeletal muscle cell, which was branched out and connected each other at terminal with striation, intercalated disk and nucleus at center of cell. 2. In MT stain of control group, a few of collagen fibrile were seen at periva scular interstium, but wasn't seen between skeletal muscle fiber, and cardiac muscle was seen in various size. 3. In MT stain of experimental group, increased collagen fiber deposition at perivascular interstiums were seen periodically. 4. In MT stain of experimental group, increased collagen fiber deposition at interstitial matrix between perimyocardiac cells were seen at 3 day, 4 weeks and 6 weeks after DM induction. 5. In H&E stain of experimental group, partial degeneration of myocardiac cells was seen after 4 weeks of DM induction. From above results, streptozotocin induced diabetes mellitus increased collagen around perivascular and between intercellular matrix in heart.

• Journal of Society of Preventive Korean Medicine
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• v.5 no.1
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• pp.116-133
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• 2001

Antifibrotic drugs could be delayed or inhibited massive collagen deposition in liver tissue or inhibited collagen synthesis. we investigated antifibrotic effects by several herbs(Schisnadra chinensis, Ganoderma japonicum, Sedum sarmentosum, Alisma canaliculatum, Plantago asiatica) extract with observations of collagen accumulation in liver tissue and collagen synthesis in sera. Rats were used for experimental animal that were devided 3 groups(sham control, BDL/S, BDL/S-ER). Rats were operated for inducing liver fibrosis(cirrhosis) by bile duct obstruction. Several herbs were prepared by water extraction and were applicated p. o. $3ml/day$ during 4 weeks. After observation period, rats were sacrificed and liver tissue and sera were collected. In result, the mortality of rats was 35% in BDL/S group and 20% in BDL/S-ER The color of bile juice in BDL/S-ER was bright yellow and murky yellow in BDL/S group. The significantly lower weight of liver($16.21g{\pm}5.3,\;20.58{\pm}2.4$) and spleen($1.96g{\pm}0.96,\;3.93{\pm}0.21$) were shown in BDL/S-ER than that of BDL/S(p<0.05) group. The value of collagen in liver tissue(25.7%) in BDL/S-ER was observed significantly lower than that of BDL/S group (Tab. 2). AST. ALT, ALP, t-bilirubin, BUN levels were low in BDL/S-ER as compared with those of BDL/S group, but the significance was not proven. The trichrome stained liver tissue in BDL/S-ER group was observed mild bile duct proliferation and fibrosis compared with BDL/S group. In conclusion, natural products inhibited new collagen synthesis and delayed massive collagen deposition in liver tissue, so that they have noticeable antifibrotic effects in experimental liver fibrosis(cirrhosis).

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.113.3-114
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• 2003

The increased deposition of extracellular matrix by hepatic stellate cells following liver injury in a process known as activation is considered a key mechanism for increased collagen content of liver during the development of liver fibrosis. In this study, we investigated the protective effects of an aqueous extract from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil (CK), on hepatic fibrosis in hepatic stellate cells. We report that CK reduces the accumulation of collagen in acetaldehyde-induced hepatic stellate cells. (omitted)

• Korean Journal of Head & Neck Oncology
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• v.13 no.2
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• pp.180-186
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• 1997

Objectives: Salivary gland tumors pose considerable difficulty in diagnostic and prognostic assessment based on the histopathologic features alone. We studied the expression of type IV collagen and fibronectin in salivary gland tumors with special emphasis on the differential diagnostic significance. Materials and Methods: We did immunohistochemical stain on paraffin embedded tissues of 33 benign and 24 malignant salivary gland tumors using monoclonal antibody for type IV collagen and polyclonal antibody for fibronectin. Results: 1) Well preserved linear basement membrane-like staining of type IV collagen was detected in duct-cell-derived benign salivary gland tumors. But pleomorphic adenoma exhibited a heterogeneous pattern as focal augmentation and interruption. 2) In malignant tumors, type IV collagen was distributed in an irregular, interrupted manner or completely absent. Adenoid cystic carcinomas displayed a marked staining of the basal membrane associated substances in the pseudocysts. 3) The staining pattern of fibronectin was similar to that of type IV collagen execpt more dense in the stroma. 4) Salivary gland tumors which have a prominent myoepithelial cell component revealed a particular deposition of basement membrane materials adjacent to the myoepithelial cells. Conclusion: The study of the basal membrane substances may be helpful for differential diagnosis of benign and malignant salivary gland tumors and identifying special features of salivary gland tumors such as pseudocystic pattern of adenoid cystic carcinoma. Also we think that the myoepithelial cells contribute to the formation of basement membrane materials.

• Journal of Veterinary Science
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• v.24 no.5
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• pp.69.1-69.11
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• 2023

Background: Kalkitoxin (KT) is an active lipopeptide isolated from the cyanobacterium Lyngbya majuscula found in the bed of the coral reef. Although KT suppresses cell division and inflammation, KT's mechanism of action in vascular smooth muscle cells (VSMCs) is unidentified. Therefore, our main aim was to investigate the impact of KT on vascular calcification for the treatment of cardiovascular disease. Objectives: Using diverse calcification media, we studied the effect of KT on VSMC calcification and the underlying mechanism of this effect. Methods: VSMC was isolated from the 6 weeks ICR mice. Then VSMCs were treated with different concentrations of KT to check the cell viability. Alizarin red and von Kossa staining were carried out to examine the calcium deposition on VSMC. Thoracic aorta of 6 weeks mice were taken and treated with different concentrations of KT, and H and E staining was performed. Real-time polymerase chain reaction and western blot were performed to examine KT's effect on VSMC mineralization. Calcium deposition on VSMC was examined with a calcium deposition quantification kit. Results: Calcium deposition, Alizarin red, and von Kossa staining revealed that KT reduced inorganic phosphate-induced calcification phenotypes. KT also reduced Ca⁺⁺-induced calcification by inhibiting genes that regulate osteoblast differentiation, such as runtrelated transcription factor 2 (RUNX-2), SMAD family member 4, osterix, collagen 1α, and osteopontin. Also, KT repressed Ca²⁺-induced bone morphogenetic protein 2, RUNX-2, collagen 1α, osteoprotegerin, and smooth muscle actin protein expression. Likewise, Alizarin red and von Kossa staining showed that KT markedly decreased the calcification of ex vivo ring formation in the mouse thoracic aorta. Conclusions: This experiment demonstrated that KT decreases vascular calcification and may be developed as a new therapeutic treatment for vascular calcification and arteriosclerosis.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.743-754
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• 2023

Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiac remodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovascular diseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effect post-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-β1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin and Masson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effects of Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 was explored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice and TGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiac function. Rg3-TGFBR1 had the 1.78×10^-7 M equilibrium dissociation constant based on SPRi analysis, and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1 knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulated the TGF-β1-mediated CFs growth together with collagen production in vitro through TGFBR1 signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferation along with collagen deposition by inactivation of TGFBR1 pathway.