• Korean Journal of Veterinary Research
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• v.18 no.2
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• pp.87-95
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• 1978

Election microscopic investigation were conducted on the mature mouse (B.W. about 25g) liver which was treated with Ginseng water extract during three, six and nine days respectivelly after carbon tetracholride injection into abdominal cavity. The results obtained were as follows: The liver cells of control group treated with carbon tetrachloride alone were restored slowly. The liver cells of experimental group treated with Ginseng water extract after carbon tetrachloride injection, however, were shown the appearance of well-developed ${\gamma}-ER$ and Golgi complex, marked aggregation of glycogen particles, and a number of large lipid droplets which are attached markedly with glycogen particles as compared to the control group. As these findings, it could be suggested that Ginseng gives an activation to restore the damaged liver cells.

• The Korean Journal of Physiology
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• v.3 no.2
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• pp.17-23
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• 1969

Oxygen consumption rate $(QO_2)$ and protein content of liver and kidney of the Ehrlich ascites tumor-bearing mouse were measured from 6th till 14th day after the inoculation of $4{\times}10^6$ Ehrlich ascites tumor cells. The results thus obtained were compared with those of the groups in which; 1) Whole body x-irradiation with 400 r was done to mouse prior to the inoculation of $4{\times}10^6$ Ehrlich ascites tumor cells, 2) Same number of the irradiated tumor cells were inoculated after subjecting the tumor cells to x-irradiation with 400 r or 900 r in vitro, and 3) the normal, and the following results were obtained; 1. $QO_2$ of the liver and kidney of the tumor-bearing mouse were all lower than the normal and a gradual decrease of $QO_2$ in both liver and kidney was noted as the ascites tumor was progressively developing. 2. In the groups where whole body x-irradiation with 400 r was done, or x-irradiation of ascites tumor cells in vitro with either 400 r or 900 r, $QO_2$ of the liver and kidney were lower than the normal, and the pattern of the decrease was similar in the case of the tumor-bearing mouse. 3. Protein contents in all the groups showed lower values than the normal, and the decrease was gradual as the ascites tumor was developing. 4. $QO_2$ and protein levels in the liver were generally lower than those in the kidney. 5. A certain cancerous metabolism was, therefore, noted in the remote organs of Ehrlich ascites tumor-bearing animal.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.4
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• pp.519-526
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• 2012

Recently, herbal flavonoids have been implicated for anti-cancer therapy. Flavonoids as a commonly known for their anti-oxidant activity, are contained in the herbal medicine as well as root of plants, vegetables, fruits, grains, tea, and wine. Kaempferol, a component of Polygonati rhizoma, a member of the herbal flavonoids, has been studied for anti-hypercholesterol, anti-hypertension and anti-diabetes. It is also known to be effective in anti-cancer therapy for breast, prostate and other type of cancers. However, the anti-cancer therapeutic mechanisms are pooly understood. Here, we investigated the molecular mechanism underlying kaempferol-induced anti-cancer effects using the human liver cancer cell lines, Hep3B, HepG2, and Sk-Hep-1, and human Chang liver cell as a control. As shown by the FACS analysis, measurement of caspase activity, DAPI and trypan blue staining, and DNA fragmentation assay, kaempferol induced apoptosis in the liver cancer cells with the greater potential in Hep3B cells than other liver cancer cells. In addition, we performed microarray analysis to profile the genome-wide mRNA expression regulated by kaempferol. Many of the apoptosis-related genes were significantly induced in kaempferol-treated Hep3B cells, in particular, the genes associated with MAPK cascade. Additionally, kaempferol induced the mRNA expression of genes involved in MKK7-JNK cascade, MKK3-p38 cascade, and caspase signaling pathway, which are all known to trigger apoptosis. Overall, our data suggest that kaempferol has anti-liver cancer effects by inducing apoptosis through the MKK7-JNK cascade, MKK3-p38 cascade, and caspase signaling pathways.

• BMB Reports
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• v.56 no.2
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• pp.65-70
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• 2023

Prominin-1 (PROM1), also called CD133, is a penta-span transmembrane protein that is localized in membrane protrusions, such as microvilli and filopodia. It is known to be expressed in cancer stem cells and various progenitor cells of bone marrow, liver, kidney, and intestine. Accumulating evidence has revealed that PROM1 has multiple functions in various organs, such as eye, tooth, peripheral nerve, and liver, associating with various molecular protein partners. PROM1 regulates PKA-induced gluconeogenesis, TGFβ-induced fibrosis, and IL-6-induced regeneration in the liver, associating with Radixin, SMAD7, and GP130, respectively. In addition, PROM1 is necessary to maintain cancer stem cell properties by activating PI3K and β-Catenin. PROM1-deficienct mice also show distinct phenotypes in eyes, brain, peripheral nerves, and tooth. Here, we discuss recent findings of PROM1-mediated signal transduction.

• Development and Reproduction
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• v.27 no.4
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• pp.167-174
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• 2023

Development of hepatocellular carcinoma (HCC) is driven by a multistep and long-term process. Because current therapeutic strategies are limited for HCC patients, there are increasing demands for understanding of immunotherapy, which has made technological and conceptual innovations in the treatment of cancer. Here, I discuss HCC immunotherapy in the view of interaction between liver resident cells and immune cells.

• Korean Journal of Environmental Biology
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• v.36 no.4
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• pp.498-506
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• 2018

The purpose of this study is to examine the restorative effect of Semisulcospira libertina extract, on damaged liver cells induced by D-galactosamine in rats. Treatment of damaged liver cells with S. libertina extract significantly reduced local fatty degeneration, and inflammatory cell necrosis, to levels similar with the undamaged control group. In addition, S. libertina extracts were found to reduce plasma levels of liver damage indicator enzymes, such as AST, ALT, LDH and ALP, to control levels. It also reduced lipid peroxides, and lipid contents within damaged liver tissues. This suggests that S. libertina extract has a restorative effect on liver cells, thus reducing release of damage-associated liver enzymes, and oxidative degradation of lipids. Also, S. libertina extracts were found to be involved in recovery of damaged cells from inflammatory response by suppressing expression of $TNF-{\alpha}$, which leads to tissue injury and necrosis, whereas inducing expression of HO-1 that protects cells during inflammation. Thus, S. libertina extract restores liver tissue from necrosis and fibrosis, as well modulates expression of inflammation-related genes against liver damage. Our findings suggest that S. libertina extract is an effective medicinal resource, for improving and recovering liver cells from hepatic injury.

• The Korean Journal of Cytopathology
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• v.1 no.1
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• pp.18-26
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• 1990

CT guided percutaneous fine-needle aspiration (FNA) of the liver for both cytologic and histologic examination has great value in diagnosing liver malignancy. From March, 1986 to April, 1990, 62 patients with the clinical impression of liver malignancy underwent CT guided percutaneous FNA biopsy. Of these, 43 cases were reviewed for this study, 19 were reported to be liver cell carcinoma, 2 were adenocarcinoma, 11 were reported as anaplastic cell present, and the rest (11 cases) were negative (9) or necrotic (2). Among the 11 cases of the last group, 9 were diagnosed as liver cell carcinoma and 2 were necrotic histologically. Retrospective review, in order to clarify the cause of cytologic diagnostic error, of both cytologic and histologic slides of all cases showed discordance of 23% between these diagnoses and sensitivity is 93.9% and specificity is 90.9%. The reasons were as follows ; 1) the lack of awareness of tumor cells of well differentiated liver cell carcinoma (4 cases), 2) missed tumor cells due to too scanty cellularity (1 case), 3) improper smear (2 cases) and no tumor cell In the cytologic smears (3 cases). In such cases, at the initiation of FNA, a correct diagnosis of liver malignancy could only be made by a combination of cytologic and histologic examinations. However after three years' experience we can conclude that cytomorphologic features of liver cell carcinoma are sufficiently distinctive from other liver malignancies to be diagnostic.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1349-1353
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• 2012

Increasing evidence has revealed that thy-1 was a potential stem cell marker of liver cancer, but no data have been shown on how thy-1 regulates the pathophysiology of liver cancer, such as proliferation, apoptosis, invasion and migration. We previously demonstrated that thy-1 was expressed in about 1% of hepg2 cells, thy-1+hepg2 cells, but not thy-1-, demonstrating high tumorigenesis on inoculation $0.5{\times}10^5$ cells per BACA/LA mouse after 2 months. In the present study, our results showed that higher expression of thy-1 occurs in 72% (36/50 cases) of neoplastic hepatic tissues as compared to 40% (20/50 cases) of control tissues, and the expression of thy-1 is higher in poorly differentiated liver tumors than in the well-differentiated ones. In addition, thy-1 expression was detected in 85% of blood samples from liver cancer patients, but none in normal subjects or patients with cirrhosis or hepatitis. There was a significant negative correlation between thy-1expression and E-cadherin expression (a marker of invasion and migraton), but not between thy-1 expression and AFP expression in all the liver cancer and blood samples. We further investigated the relationship between thy-1 and E-cadherin in liver cancer hepg2 cell line which was transfected with pReceiver-M29/thy-1 eukaryotic expression vector followed by aspirin treatment. Lower expression of E-cadherin but higher expressions of thy-1 were detected in hepg2 cells transfected with pReceiver-M29/thy-1. Taken together, our study suggested that thy-1 probably regulates liver cancer invasion and migration.

• Korean Journal of Veterinary Research
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• v.29 no.4
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• pp.531-540
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• 1989

A new sudden death in rabbits appeared in China and Korea in 1984 and 1985, respectively, and was recognized to be an acute infectious disease caused by a virus. The disease was reported as a "new viral disease," and thereafter, a tentative name of "viral hemorrhagic disease", "hemorrhagic pneumonia" or "viral hemorrhagic pneumonia" has been described in the case reports. But authors had called the viral disease "rabbit viral hepatitis" due to picornavirus infection, because the principal lesion of the disease was an acute hepatitis. The purpose of this report is to describe the electron microscopic findings on the livers in experimentally infected rabbits. All the livers of the affected rabbits were shown to have degenerative changes of a type that is characteristic of acute hepatitis. In the liver cells, there were dilation of rER and mitochondria, vacuole formation of various sizes, and appearances of many virus-like particles in the vicinity of rER, granular bodies and crystalline arrays of viral particles in the cytoplasm with necrotic changes of the nucleus. Clusters of virus-like particles and viral crystals appeared in the cytoplasm of sinusoid endothelial cells and Kupffer's cells with morphological changes of organelles. Also viral crystals were demonstrated in the cytoplasm of macrophages among the liver cells. On the whole, the liver cells had many virus-like particles and a few crystalline arrays of viral particles. Therefore, this implies that the liver cells are the main site of the viral replication in inducing the viremia. It was concluded that the liver was the primary target organ of this viral disease, and the pathological and the ultrastructural evidence suggest that the virus may be belong to genus enterovirus.

• Journal of Physiology & Pathology in Korean Medicine
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• v.38 no.1
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• pp.10-15
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• 2024

Previous studies have highlighted the pivotal role of the β-adrenergic receptor (β-AR) signaling pathway in stimulating cancer metastasis induced by chronic stress. According to the theory of traditional Korean medicine, chronic stress can induce Qi stagnation. Based on the traditional role of premature citrus unshiu peel in moving Qi, we hypothesized that an ethanol extract of premature citrus unshiu peel (EPCU) can attenuate chronic stress-induced cancer progression. In this study, we investigated the potential role of EPCU on modulating the adrenergic agonists-induced metastatic properties of liver cancer cells. Our findings revealed that adrenergic agonists, including norepinephrine (NE), epinephrine (E), and isoproterenol (ISO), augmented the migratory capacity of Hep3B human hepatocellular carcinoma cells, which was completely abrogated by EPCU treatment in a concentration-dependent manner. Consistently, EPCU inhibited the E-induced invasive property of Hep3B cells in a dose-dependent manner. These results suggest that EPCU efficiently attenuates adrenergic agonists-induced metastatic abilities of liver cancer cells. As a molecular mechanism, EPF suppressed the phosphorylation of major components of β-AR signaling pathway, including Src, signal transducer and activator of transcription 3 (STAT3) and ERK, induced by E treatment. Taken together, our results demonstrate that EPCU impedes the adrenergic agonists-driven metastatic potential of cancer cells by inhibiting β-AR signaling pathway. This study provides basic evidence supporting the probable use of premature citrus unshiu peel to prevent metastasis in liver cancer patients under chronic stress.