• 한국간담췌외과학회지
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• 제26권4호
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• pp.325-332
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• 2022

Backgrounds/Aims: To analyze relationships of hepatic histopathological findings and bile microbiological profiles with perioperative outcomes and risk of late biliary stricture in individuals undergoing surgical bile duct injury (BDI) repair. Methods: A historical cohort study was carried out at a tertiary university hospital. Fifty-six individuals who underwent surgical BDI repair from 2014-2018 with a minimal follow-up of 24 months were enrolled. Liver biopsies were performed to analyze histopathology. Bile samples were collected during repair procedures. Hepatic histopathological findings and bile microbiological profiles were then correlated with perioperative and late outcomes through uni- and multi-variate analyses. Results: Forty-three individuals (76.8%) were females and average age was 47.2 ± 13.2 years; mean follow-up was 38.1 ± 18.6 months. The commonest histopathological finding was hepatic fibrosis (87.5%). Bile cultures were positive in 53.5%. The main surgical technique was Roux-en-Y hepaticojejunostomy (96.4%). Overall morbidity was 35.7%. In univariate analysis, liver fibrosis correlated with the duration of the operation (R = 0.3; p = 0.02). In multivariate analysis, fibrosis (R = 0.36; p = 0.02) and cholestasis (R = 0.34; p = 0.02) independently correlated with operative time. Strasberg classification independently correlated with estimated bleeding (R = 0.31; p = 0.049). The time elapsed between primary cholecystectomy and BDI repair correlated with hepatic fibrosis (R = 0.4; p = 0.01). Conclusions: Bacterial contamination of bile was observed in most cases. The degree of fibrosis and cholestasis correlated with operative time. The waiting time for definitive repair correlated with the severity of liver fibrosis.

• 대한의생명과학회지
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• 제28권2호
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• pp.101-108
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• 2022

High-fat diet (HFD)-fed ovariectomized (OVX) female mice were used as an animal model of obese postmenopausal women. We investigated the effects of ascorbic acid on the histological changes induced in the liver. Plasma alanine aminotransferase levels and liver weights were higher in mice fed an HFD for 18 weeks than in mice fed a low-fat diet, effects that were inhibited by ascorbic acid. Similarly, mice fed an ascorbic acid-supplemented HFD had less hepatic lipid accumulation than did mice fed an HFD alone. Moreover, administration of ascorbic acid reduced inflammatory cells, including mast cells and CD68-positive cells, and inflammatory foci in the liver and inhibited hepatocyte ballooning. Hepatic collagen levels were lower in ascorbic acid-treated versus non-treated mice. These results suggest that ascorbic acid inhibits hepatic steatosis, inflammation, and fibrosis in obese OVX mice. Thus, ascorbic acid intake may be useful for postmenopausal women with nonalcoholic fatty liver disease.

• Toxicological Research
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• 제26권3호
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• pp.193-201
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• 2010

Hepatic fibrosis represents the main complication of most chronic liver disorders and, regardless of its etiology, is characterized by excessive deposition of extracellular matrix components. In this study, we examined that 1-O-Hexyl-2,3,5-Trimethylhydroquinone (HTHQ), a potent anti-oxidative agent, could prevent experimental hepatic fibrosis induced by dimethylnitrosamine (DMN) in male SD rats. Except for vehicle control group, other groups were induced hepatic fibrosis by intraperitoneal injection with DMN (10 mg/ml/kg) on 3 consecutive days weekly for 4 weeks. During the same 4 weeks, control and DMN groups were given vehicle and HTHQ 50, 100 and 200 groups were orally administered HTHQ (50, 100, 200 mg/kg respectively). In HTHQ 100 and 200 groups, relative liver weight and serum chemistry level improved significantly. HTHQ reduced hydroxyproline (p < 0.05) and malondialdehyde (p < 0.05) level in the liver. Histopathological examination of H&E, Masson's trichrome stain showed the reduced fibrotic septa in HTHQ 100 and 200 groups. HTHQ administration showed reduced mRNA level of PDGF (Platelet-derived growth factor), $\alpha$-SMA ($\alpha$-smooth muscle actin) and TGF-$\beta$ (transforming growth factor-$\beta$) than DMN-induced hepetic fibrosis animals in the liver tissue. In this study, we showed that HTHQ improves against DMN-induced liver fibrosis in male SD rats.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.172.2-173
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• 2003

Naringenin, a phytoalexin found in grapefruit. has been reported to exhibit a wide range of pharmacological properties. The aim of the present study is to evaluate the protective effect of naringenin on hepatic fibrosis induced by dimethylnitrosamine (DMN) in rats. Fibrosis was induced by intraperitoneal injection of DMN. Naringenin was given orally at 20 mg/kg and 50 mg/kg daily for 4 weeks. (omitted)

• 동아시아식생활학회지
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• 제23권1호
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• pp.44-52
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• 2013

This study investigated hepatic functional improvement and anti-fibrotic effects of water extracts of black tea. Male Sprague-Dawley rats were divided into four groups (normal, control, and two experimental subgroups: Ba, Bb) and observed for 3 weeks. Liver fibrosis in rats developed from carbon tetrachloride ($CCl_4$) administration, except for the normal group. Except for the normal and control group, the two experimental subgroups were fed water extracts of black tea. The food efficiency ratio significantly increased in the experimental group compared to the control group. The experimental group had a significantly lower liver weight compared to the control group. The ratio of liver weight to body weight was significantly lower in the experimental group than the control group. The levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, blood urea nitrogen, and low-density lipoprotein-cholesterol in serum significantly decreased in the experimental group compared to the control group. The values of hydroxyproline and malondialdehyde in liver were even lower in the experimental group than the control group. In observations on liver histology, weaker inflammation and fibrosis were observed in the experimental group compared to the control group. In conclusion, water extracts of black tea help hepatic cells keep their functions, restraining and protecting the liver from impairments caused by $CCl_4$ administration, and can be effective as anti-fibrotic agents.

• Journal of Applied Biological Chemistry
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• 제59권1호
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• pp.25-29
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• 2016

B형 간염 바이러스는 간경변증과 간세포암의 원인이 되는 간섬유화를 유발한다. 하지만 현재까지 그와 관련한 자세한 메커니즘은 밝혀지지 않았기에 본 연구에서 이를 알아보고자 하였다. 실험 결과, B형 간염 바이러스에서 발현되는 HBx 단백질에 의해 vimentin, fibronectin, slug, snail, NOX4가 증가되는 것을 확인하였다. NOX4에 의한 활성산소가 snail, slug 발현을 유도하고 섬유화 과정을 촉진할 수 있기 때문에 NOX4의 발현을 유도하는 HBx가 간섬유화를 조절, 유도하는 것을 확인하였다.

• 동의생리병리학회지
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• 제17권5호
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• pp.1264-1269
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• 2003

The inhibitory effects of the Juglans sinensis walnut ethanol extract (JSWE) on carbon tetrachloide (CCl₄)-induced fibrosis, serum transaminases (GOT and GTP), hepatic glutathione (GSH), serum pro-inflammatory cytokines (IL-1β and IL-6) were investigated in rats. JSWE significantly inhibited on CCl₄-induced fibrosis in dose-dependent manner. Moreover, JSWE significantly inhibited on the serum levels of GOT, GTP, IL-1β, and IL-6 in dose-dependent manner in CCl₄-induced fibrosis rat. However, JSWE markedly increased the production of hepatic GSH in a dose-dependent manner. These results show that JSWE may explain some known biological activities of Juglans sinensis walnut including their anti-fibrotic and anti-inflammatory effects, and is of considerable benefit in the treatment for live diseases.

• Biomolecules & Therapeutics
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• 제28권1호
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• pp.92-97
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• 2020

A previous pharmacogenomic analysis identified cromolyn, an anti-allergic drug, as an effective anti-fibrotic agent that acts on hepatocytes and stellate cells. Furthermore, cromolyn was shown to be a G protein-coupled receptor 35 (GPR35) agonist. However, it has not been studied whether anti-fibrotic effects are mediated by GPR35. Therefore, in this study, the role of GPR35 in hepatic fibrosis was investigated through the use of lodoxamide, another anti-allergic drug and a potent GPR35 agonist. Long-term treatment with carbon tetrachloride induced hepatic fibrosis, which was inhibited by treatment with lodoxamide. Furthermore, CID2745687, a specific GPR35 antagonist, reversed lodoxamide-mediated anti-fibrotic effects. In addition, lodoxamide treatment showed significant effects on the mRNA expression of collagen Iα1, collagen Iα2, and TGF-β1 in the extracellular matrix. However, a transforming growth factor α (TGF-α) shedding assay revealed lodoxamide not to be a potent agonist of mouse GPR35 in vitro. Therefore, these results showed anti-fibrotic effects of lodoxamide in mice and raise concerns how lodoxamide protects against liver fibrosis in vivo and whether GPR35 is involved in the action.

• Clinical and Experimental Pediatrics
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• 제45권7호
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• pp.923-927
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• 2002

우연히 발견된 간비장 종대를 주소로 내원한 3세 여아에서 신낭종을 동반한 선천성 간섬유화증을 진단한 예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

• 한국수의병리학회:학술대회논문집
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• 한국수의병리학회 2003년도 추계학술대회초록집
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• pp.16-16
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• 2003

Hepatic fibrosis is a common response to various chronic hepatic injuries and occurs as a consequence of the transformation of hepatic stellate cells into myofibroblasts (MFBs) producing abnormal extracellular matrix which is mainly induced by transforming growth factor-beta (TGF-${\beta}$), especially TGF-${\beta}$1 [1,2]. As the liver becomes fibrotic, there are both quantitative and qualitative changes in several pathological markers related to the hepatic fibrosis. These fibrotic markers in liver are mainly consisted of several proteins and cytokines, but sometimes included specific type cells. The aim of this study was to detect expression and change of markers (TGF-${\beta}$, mallory body, cytokeratin, ${\alpha}$-SMA, hypoxia, collagen) during hepatic fibrogenesis. (omitted)