• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.519-529
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• 2011

Objectives : This study was performed to investigate the effects of Injinchunggan-tang on cell growth and apoptosis in human hepatic stellate cell line LX2. Materials and Methods : Hepatic stellate cells were treated with various concentrations of Injinchunggan-tang extract for 24, 48 and 72 hours. The extraction was done with distilled water. After the treatment, cell viability, proliferation, apoptosis, caspase activity, caspase inhibitor and the mRNA of the Bcl-2, and Bax with ${\beta}$-actin were measured by using MTT assay, apoptosis assay and RT-PCR. Results : Proliferation, and mRNA expression of the hepatic stellate cells were inhibited by Injinchunggan-tang treatment in a dose-dependent manner. This indicates the prescription has inhibitory effect on fibrogenesis of the liver by regulating the fibrogenesis-associated genes in transcription. Cell viability was inhibited in time- and dose-dependent manners. Conclusions : These results suggest that Injinchunggan-tang would be beneficial in the treatment of cirrhotic patients as well as for the patients with chronic hepatitis.

• 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)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.167-167
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• 2003

Hepatic stellate cells (HSC) and the derived myofibroblasts are known to playa central role in liver fibrosis. Rhus verniciflua Strokes (RVS) has traditionally been used in Korea herbal medicine for a stomachic tonic. In this study, we observed the effect of RVS acetone extract (Ra) on the proliferation, the collagen synthesis, and hepatic fibrosis related proteins mRNA levels in HSC-T6 cells which is a fully acivated rat hepatic stellate cell line.(omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.142.2-142.2
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• 2003

The activation of the hepatic stellate cell (HSC) is a key step in liver fibrogenesis. We investigated the changes of global gene expression during activation in hepatic stellate cells using a rat cDNA microarray with 5, 000 sequence-verified clones. We identified osteopontin (OPN), a secreted matrix protein, as one of the upregulated factors. Northern analysis showed OPN mRNA was increasingly expressed during progressive activation of cultured rat HSCs and in models of experimental liver fibrosis. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.103.3-104
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• 2003

Activation of hepatic stellate cell has been identified as a critical step in hepatic fibrogenesis and is regulated by several factors including cytokines and oxidative stress. In this study, we assayed effects of saponin (CKS), inulin (CKI) and oligo-sugars (CKO) isolated from Platycodon grandiflorum A. DC, changkil (CK) on experimental cell cycle arrest and apoptosis in hepatic stellate cell line (HSC-T6). CKS induced cell arrest at G$_1$. CKS also reduced intercellular reactive oxygen species and collagen synthesis in hydrogen peroxide-induced oxidative stress and acetaldehyde-stimulated collagen synthesis, respectively, in HSC-T6 cells. (omitted)

• Biomolecules & Therapeutics
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• v.31 no.4
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• pp.425-433
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• 2023

During liver injury, hepatic stellate cells can differentiate into myofibroblast-like structures, which are more susceptible to proliferation, migration, and extracellular matrix generation, leading to liver fibrosis. Anaerobic glycolysis is associated with activated stellate cells and glyceraldehyde (GA) is an inhibitor of glucose metabolism. Therefore, this study aimed to investigate the anti-fibrotic effects of GA in human stellate LX-2 cells. In this study, we used cell viability, morphological analysis, fluorescence-activated cell sorting (FACS), western blotting, and qRT-PCR techniques to elucidate the molecular mechanism underlying the anti-fibrotic effects of GA in LX-2 cells. The results showed that GA significantly reduced cell density and inhibited cell proliferation and lactate levels in LX-2 cells but not in Hep-G2 cells. We found that GA prominently increased the activation of caspase-3/9 for apoptosis induction, and a pan-caspase inhibitor, Z-VAD-fmk, attenuated the cell death and apoptosis effects of GA, suggesting caspase-dependent cell death. Moreover, GA strongly elevated reactive oxygen species (ROS) production and notably increased the phosphorylation of ERK and JNK. Interestingly, it dramatically reduced α-SMA and collagen type I protein and mRNA expression levels in LX-2 cells. Thus, inhibition of ERK and JNK activation significantly rescued GA-induced cell growth suppression and apoptosis in LX-2 cells. Collectively, the current study provides important information demonstrating the anti-fibrotic effects of GA, a glycolytic metabolite, and demonstrates the therapeutic potency of metabolic factors in liver fibrosis.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.504-518
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• 2011

Objectives : This study was performed to investigate the anti-fibrogenic effect of greater celandine on cultured rat hepatic stellate cells. Materials and Methods : Hepatic stellate cells (HSC-T6) were treated with various concentrations of greater celandine extract for 24, 48, and 72 hours. The extraction was done with distilled water. After the treatment, cell viability, proliferation, mRNA of the ${\alpha}SMA$, TIMP-1, TIMP-2, collagen I ${\alpha}$ 1, MMP-2, IL-6, TGF-${\beta}1$, PDGFr-${\beta}1$, Bcl-2, Bax, Bcl-xl, caspase-3, caspase-9 and the activities of SOD and catalase were measured by using MTT assay, BrdU assay, real-time PCR, superoxide dismutase assay and catalase assay. Results : The viability, proliferation, mRNA expression and synthesis of collagen of the hepatic stellate cells were inhibited as the concentration increased, which indicates the herb has an inhibitory effect on fibrogenesis of the liver by regulating the fibrosis associated genes in transcription. Conclusions : These results suggest that greater celandine would be beneficial in the treatment of fibrotic patients as well as for patients with chronic hepatitis.

• The Journal of Internal Korean Medicine
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• v.26 no.4
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• pp.853-863
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• 2005

Object : This study was performed to investigate the anti-fibrogenic effect of Artemisiae Capillaris Herba(ACH) on cultured rat hepatic stellate cells. Methods : Hepatic Stellate Cells were obtained from a 350gm Sprague-Dawley rat by tissue perfusion system, and the cells for the study were selected after 3 passages of culture on non-coated plastic culture dishes which enable the cells to activate, thus producing collagens in the cell media. Cells were treated with various concentrations of Artemisia Capillaris Herba(ACH) extract powder for 24 or 48 hours. After the treatment, Soluble collagen, procollagen levels and the mRNA of the procollagen type I C were measured by using assay kit and RT-PCR method. Results : Procollagen production by the hepatic stellate cells decreased after the treatment in a time-dependent dose-dependent manner. The mRNA expression decreased consistently with the volume of the secreted procollagen which indicates the herb hat inhibitory effect on fibrogenesis of the liver by regulating one of the fibrosis associated genes in transcription. Conclusion : These results suggest that ACH is beneficial in the treatment of cirrhotic patients as well as for the patients with chronic hepatitis.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.138-143
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• 2023

Liver fibrosis is caused by metabolic problems such as cholestasis, genetic problems, or viral infections. Inhibiting hepatic stellate cell (HSC) activation or inducing selective apoptosis of activated HSCs is used as a treatment strategy for liver fibrosis. It has been reported that when HSCs are activated, their apoptosis sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is enhanced because the expression of death receptor 5 is elevated. Finding a natural compound that can enhance the apoptotic effect of TRAIL on HSCs is a necessary strategy for liver fibrosis treatment. It was confirmed here that mangosteen-derived gartanin increased the effect of TRAIL-induced apoptosis by increasing the expression of DR5 in a p38-dependent manner in the hepatic stellate cell line LX-2. Combined treatment with gartanin and TRAIL accelerated DNA cleavage through caspase-3 activation and enhanced antifibrotic effects in LX-2 cells.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.238.1-238.1
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• 2003

Hepatic stellate cells (HSC) and the derived myofibroblasts are known to play a central role in liver fibrogenesis. Rhus verniciflua Strokes (RVS) has traditionally been used in Korea herbal medicine for a stomachic tonic. In this study, we observed the effect of RVS acetone extract (Ra) and its five major components on the proliferation, the collagen synthesis, and hepatic fibrosis related proteins mRNA levels in HSC-T6 cells which is a fully activated rat hepatic stellate cell line. Ra inhibited the proliferation and decreased the content of collagen in the HSC-T6 cells. (omitted)