• The Journal of Internal Korean Medicine
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• v.29 no.2
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• pp.299-310
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• 2008

Objectives : This study was performed to investigate the anti-fibrogenic effect of Salvia miltiorrhiza on rat hepatic stellate cells. Materials and Methods : Hepatic stellate cells(HSC-T6) were treated with various concentrations of Salvia miltiorrhiza extract for 24 hours. It was extracted either with distilled water or 50% EtOH. After the treatment, cell viability, proliferation, procollagen levels and the mRNA of the collagen type 1a2 and ASMA were measured Results : The viability and proliferation of the hepatic stellate cells were decreased as concentration increased. The mRNA expression decreased consistently with the volume of the secreted procollagen with the extraction made with distilled water. This indicates the herb has inhibitory effect on fibrogenesis of the liver by regulating one of the fibrosis associated genes in transcription. However it increased in 50% EtOH extraction, which shows that a more stable reaction is expected of the extraction made with distilled water than the extraction made with 50% EtOH. The production of procollagen was decreased by a low-concentration treatment with Salvia miltiorrhiza, but increased by a high concentration. It seemed that the cells were responding to Salvia miltiorrhiza in low- concentration, thus producing smaller amounts of collagen. When the drug was administered in high enough concentration to give direct toxicity to cells, an overproduction of collagen was observed. Conclusion : These results suggest that Salvia miltiorrhiza is a possible candidate for the treatment of cirrhotic patients as well as for patients with chronic hepatitis when extracted with water in the proper concentrations.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.3
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• pp.380-386
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• 1994

The behavior of glycogen and histological changes of hepatic tissues in the liver of rats, aged 6 to 7 weeks, fed 18% casein diet under control, gramoxone and gramoxone + vitamin C(Vt. C) diets has been investigated in a comined histropathological and histochemical studies. Cloudy swelling and fat changes of hepatic cells were observed in the gramoxone group with the duration of feeding time. Fat changes of hepatic cells were observed more obviously than cloudy welling, especially in the hepatic cells of periportal area. The number of Kupffer's cells increased signifciantly in the gramoxone group fed for 4weeks. The cloudy swelling and fat changes decreased obviously in the gramxone + Vt. C group. Glycogen content of heaptic cells tended to increase slightly in the gramoxone group as compared with the control group . moreover, glycogen depositons were higher in the hepatic cells where fat changes were obvious. It seems to be that Vt.C alleviating effects on the gramoxone toxicity in the patterns of glycogen distribution and histological structure of heaptic tissues.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6341-6345
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• 2013

To clarify the role of stem cells in hepatocarcinogenesis, glypican-3 (GPC-3) and E-cadherin expression was investigated in embryonic cell lineages. Mouse embryonic stem cells (ESCs), hepatic progenitor cells (HPCs) and hepatocyte like cells (HCs), representing 0, 22 and 40 days of differentiation, respectively, were treated in vitro with diethylnitrosamine (DEN) at four doses (0, 1, 5 and 15 mM; G1, G2, G3 and G4, respectively) for 24 h and GPC-3 and E-cadherin expression was examined by relative quantitative real-time PCR and immunocytochemistry. GPC-3 mRNA expression was significantly different for G4 at day 0 (p<0.001) and for G4 at day 22 (p<0.01) compared with the control (G1). E-cadherin mRNA expression was significantly different for G3 and G4 at day 0 (p<0.05 and p<0.001, respectively), for G2 and G4 (p<0.05 and p<0.001, respectively) at day 22 and for G2 and G4 (p<0.01 and p<0.001, respectively) at day 40 compared with G1. Immunofluorescence staining for GPC-3 showed a membranous and/or granular expression in cytoplasm of ESCs and HPCs and granular and/or diffuse expression in cytoplasm of HCs, which were also stained by E-cadherin. DEN treatment increased GPC-3 expression in ESCs, HPCs and HCs, with increase of E-cadherin expression. Taken together, the expression of GPC-3 was altered by DEN treatment. However, its expression pattern was different at the stage of embryo stem cells and its derived hepatic lineage cells. This suggests that GPC-3 expression may be modulated in the progeny of stem cells during their differentiation toward hepatocytes, associated with E-cadherin expression.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.3
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• pp.246-248
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• 2008

A hepatic angiomyolipoma is a rare benign tumor mainly composed of blood vessels, smooth muscle cells and fat cells in varying proportion. Hepatic angiomyolipoma is often misdiagnosed as a hepatocellular carcinoma in preoperative imaging work-up. To date, there has been little published data describing PET findings of hepatic angiomyolipoma. We report one case of hepatic angiomyolipoma that showed a high acetate and relatively low FDG uptake on PET images.

• The Korea Journal of Herbology
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• v.26 no.3
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• pp.65-73
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• 2011

Objectives : The present study was evaluated the protective roles of Spatholobi Caulis in hepatotoxic rats due to APAP overdose. Methods : In experiments, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE; 50, 100 mg/kg) for 4 days and then, orally gavage with APAP (1.2 g/kg) to induce acute liver damage. Results : Oral injection of APAP caused severe hepatic injury. Plasma ALT, AST and LDH levels were significantly elevated, but SCE significantly decreased ALT, AST and LDH to the normal level. In histopathological analysis, peripheral hemorrhage around portal triads and central necrosis around central veins were founded after APAP treatment. However, these histopathological changes were recovered by SCE pretreatment. SCE also decreased the percentage of generative hepatic regions (%/$mm^2$ hepatic parenchyma), the numbers of inflammatory cells (cells/$mm^2$ hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cellls) which were significantly elevated after APAP injection. Furthermore, SCE down-regulated the contents of hepatic MDA and up-regulated hepatic GSH. SCE also inhibited the decrease in the expression of pro-caspase-3 by APAP treatment. Conclusions : Collectively, these data indicate that SCE protected APAP-induced hapatic damages through antioxidative and anti-apoptotic process. These findings the significant therapeutic potential of SCE during APAP-induced liver injury.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.120-120
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• 2003

• 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.

• IMMUNE NETWORK
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• v.10 no.6
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• pp.181-187
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• 2010

Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.

• Biomedical Science Letters
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• v.23 no.2
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• pp.144-153
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• 2017

It was demonstrated that Gangjihwan (DF), which is the herbal composition composed of Ephedra intermedia, Lithospermum erythrorhizon, and Rheum palmatum, inhibits obesity and hepatic steatosis in high fat diet (HFD)-fed obese mice. The aim of this study was to determine the effects of DF on visceral obesity, hepatic inflammation and fibrosis and the mechanism of actions involved in this process using in vivo and in vitro approaches. DF was extracted with water (DF-FW), 30% grain alcohol (DF-GA30), and 70% grain alcohol (DF-GA70). Administration of DF to HFD-fed control mice decreased visceral tissue mass and visceral adipocyte size without adverse effects. Visceral fat mass was decreased by DF-GA30 and DF-GA70, and visceral adipocyte size by all three DF extracts compared with obese control mice. Histological analysis revealed that three kinds of DF extracts reduced toluidine blue-stained mast cells and collagen accumulation in the liver, the extents of which were most eminent in DF-GA70-treated mice. DF-GA70 decreased the mRNA levels of the inflammation ($TNF{\alpha}$ and VCAM-1), fibrosis (${\alpha}-SMA$), and apoptosis (caspase 3) genes, but increasing the anti-apoptosis gene (Bcl-2) mRNA levels in the liver of obese control mice. Consistent with the in vivo data, GA-70 also altered the expression of inflammation genes ($TNF{\alpha}$ and MCP-1) in HepG2 cells. These results indicate that DF not only inhibits visceral obesity, but also ameliorates visceral obesity-induced hepatic inflammation and fibrosis and that this process may be mediated by regulating the hepatic expression of inflammatory and fibrogenic genes.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.2 no.2
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• pp.185-193
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• 1999

Purpose: Proliferation of bile duct-like structures and fibrosis is a hepatic cellular reaction observed in most forms of human liver disease and in a variety of experimental conditions associated with liver injury. The aim of this study was to investigate the activation of Ito cells and bile duct proliferation in the rat after common bile duct ligation (CBDL). Methods: Hepatic morphological abnormalities were examined in rats whose bile ducts had been irreversibly ligated for 15, 21, 24 and 28 days. The liver was examined by immunohistochemical staining for ${\alpha}$-smooth muscle actin, the known marker of activated Ito cells, and light and electron microscopes. Results: After CBDL, the bile canalicular proliferation and interstitial fibrosis were gradually increased in the periportal areas extended to hepatic sinusoids. Ito cells positive for ${\alpha}$-smooth muscle actin were frequently observed in the periductular space and in perisinusoidal space of Disse. Ito cells and myofibroblasts were gradually increased in the interstitial fibrosis until the 28th day after CBDL. Ito cells and myofibroblasts had microfilaments with dense body at the periphery of the cell. Conclusions: Our results suggest that Ito cells may be fibroblastic or myogenic. It has also been postulated that during the development of hepatic fibrosis, Ito cells become myofibroblasts or fibroblast like cells.