• The Korea Journal of Herbology
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• v.30 no.1
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• pp.51-57
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• 2015

Objectives : The effect of pear extract with Daekumeumjagami and vitamin C medication(PDV) on alcohol metabolism and hepatic injury was assessed following hepatic injury induced by alcohol in mice. Methods : The model of alcoholic hepatic injury was established by orally administration with 3 g/kg 25% alcohol in mice. PDV was orally administrated once a day for 5 days. Mice were randomly divided into 5 groups : normal group, control group, and PDV groups (PDV-A, PDV-B and PDV-C). The activities of aspartate amino transferase (AST) and alanine amino transferase (ALT) and alcohol dehydrogenase (ADH) in serum, superoxide dismutase (SOD) and catalase in liver were determined after alcohol exposure. Results : Compared with control group, treatment with PDV-B and PDV-C significantly elevated activities of ADH. Moreover, the index of hepatic injury in serum was significantly decreased by treatment with PDV-B and PDV-C in ALT activity and PDV-C in AST activity. Additionally, enhanced catalase activities in liver was found in PDV-C treated mice after exposure to alcohol. Also, WBC in blood was significantly lower by treatment with PDV-B and PDV-C. Conclusions : This study suggests that PDV treatment could enhance alcohol metabolism, and prevent hepatic injury after alcoholic hepatic injury and that this effect is likely related to its modulation on the alcohol metabolizing and antioxidant enzymes.

• Journal of Veterinary Clinics
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• v.34 no.3
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• pp.189-192
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• 2017

Thirteen dogs were diagnosed as congenital extrahepatic single PSS by intraoperative mesenteric portovenography or computed tomographic examination, repair surgery was performed by using an ameroid constrictor. Hepatic size was measured from the right lateral view using liver length/T11 length ratio. This measurement was performed on follow-up check of PSS ligation patients. Hepatic size parameter of pre-operative PSS patients is $4.13{\pm}0.13$ (range, 3.11-4.83). After surgery, hepatic size parameter of post-operative PSS patients is $4.79{\pm}0.19$ (range, 3.78- 5.93). Although follow-up periods varied 2 and 26 weeks, all patients showed increased liver size compared to that on pre-operative radiographs (P < 0.01). The increase rate was 1.01-1.46 times than those of preoperative radiographs. But in 5 patients, post hepatic liver size was small compared to the others, which showed low increase rate of body weight, total protein, albumin, and glucose level. It was thought that small value of hepatic size parameter was due to delay of hepatic regeneration. In conclusion, radiographic hepatic size parameter of pre- and post-operative patients is considered an effective evaluation for restoring after PSS surgery.

• Journal of Pharmaceutical Investigation
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• v.25 no.3
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• pp.193-204
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• 1995

In order to examine the effect of extrahepatic cholestasis induced by common bile duct ligation on the hepatic function, the pharmacokinetics of antipyrine and d-propranolol were investigated in rats. In addition, in an attempt to observe the degree of direct hepatic injury, light and electron microscopic observations and conventional pathologic test using serum were performed. Five days after common bile duct ligation, antipyrine(15 mg/kg) and d-propranolol(3 mg/kg) were intravenously administrated to the rats, respectively. The total clearances of antipyrine and d-propranolol were significantly(p<0.05) decreased. Because hepatic clearance of antipyrine poorly extracted by the liver and that of d-propranolol highly extracted by the liver are respectively dependent on the hepatic intrinsic clearance and the hepatic blood flow, it may be concluded that extrahepatic cholestasis following five days after common bile duct ligation decreased the hepatic intrinsic clearance and the hepatic blood flow. SGPT, SGOT, cholesterol, bilirubin(total bilirubin, direct bilirubin) and alkaline phosphatase were significantly increased(p<0.05). The proliferation of bile ducts was prominent, and degeneration and necrosis of hepatocytes were observed by light microscope. Also, ultrastructurally, bile canaliculi were containing the amorphous materials and losing microvilli, and SER and RER in hepatocytes were dilated and vacuolated.

• 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.

• Archives of Pharmacal Research
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• v.27 no.1
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• pp.111-117
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• 2004

Hepatic microcirculatory failure is a major component of reperfusion injury in the liver. Recent data provided some evidence that endothelium-derived vasoconstrictors and vasodilators may be functionally important to the control of the total hepatic blood flow under these conditions of circulatory failure. Since Kupffer cells provide signals that regulate the hepatic response in ischemia/reperfusion (I/R), the aim of this study was to investigate the role of Kupffer cells in the I/R-induced imbalance of vasoregulatory gene expression. Rats were subjected to 60 min hepatic ischemia, followed by 5 h of reperfusion. The Kupffer cells were inactivated by gadolinium chloride ($GdCl_3$, 7.5 mg/kg body weight, intravenously) 1 day prior to ischemia. Liver samples were obtained 5 hrs after reperfusion for RT-PCR analysis of the mRNA for genes of interest: endothelin-1 (ET-1), its receptors $ET_A and ET_B$, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1). ET-1 mRNA expression was increased by I/R. mRNA levels for $ET_A$ receptors showed no change, whereas $ET_B$ receptor transcripts increased in the I/R group. The increases in ET-1 and $ET_B$ mRNA were not prevented by the $GdCI_3$ pretreatment. The mRNA levels for iNOS and eNOS significantly increased within the I/R group with no significant difference between the I/R group and the $GdCl_3$-treated I/R group. HO-1 mRNA expression significantly increased in the I/R group and this increase was attenuated by $GdCI_3$. In conclusion, we have demonstrated that an imbalance in hepatic vasoregulatory gene expression occurs during I/R. Our findings suggest that the activation of Kupffer cells is not required for I/R-induced hepatic microvascular dysfunction.

• Korean Journal of Radiology
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• v.21 no.12
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• pp.1367-1373
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• 2020

Objective: To assess diffusion tensor imaging (DTI) parameters of the hepatic parenchyma for the differentiation of biliary atresia (BA) from Alagille syndrome (ALGS). Materials and Methods: This study included 32 infants with BA and 12 infants with ALGS groups who had undergone DTI. Fractional anisotropy (FA) and mean diffusivity (MD) of the liver were calculated twice by two separate readers and hepatic tissue was biopsied. Statistical analyses were performed to determine the mean values of the two groups. The optimum cut-off values for DTI differentiation of BA and ALGS were calculated by receiver operating characteristic (ROC) analysis. Results: The mean hepatic MD of BA (1.56 ± 0.20 and 1.63 ± 0.2 × 10^-3 mm²/s) was significantly lower than that of ALGS (1.84 ± 0.04 and 1.79 ± 0.03 × 10^-3 mm²/s) for both readers (r = 0.8, p = 0.001). Hepatic MD values of 1.77 and 1.79 × 10^-3 mm²/s as a threshold for differentiating BA from ALGS showed accuracies of 82 and 79% and area under the curves (AUCs) of 0.90 and 0.91 for both readers, respectively. The mean hepatic FA of BA (0.34 ± 0.04 and 0.36 ± 0.04) was significantly higher (p = 0.01, 0.02) than that of ALGS (0.30 ± 0.06 and 0.31 ± 0.05) for both readers (r = 0.80, p = 0.001). FA values of 0.30 and 0.28 as a threshold for differentiating BA from ALGS showed accuracies of 75% and 82% and AUCs of 0.69 and 0.68 for both readers, respectively. Conclusion: Hepatic DTI parameters are promising quantitative imaging parameters for the detection of hepatic parenchymal changes in BA and ALGS and may be an additional noninvasive imaging tool for the differentiation of BA from ALGS.

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.341-348
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• 2024

Endoplasmic reticulum (ER) stress plays a crucial role in liver diseases, affecting various types of hepatic cells. While studies have focused on the link between ER stress and hepatocytes as well as hepatic stellate cells (HSCs), the precise involvement of hepatic macrophages in ER stress-induced liver injury remains poorly understood. Here, we examined the effects of ER stress on hepatic macrophages and their role in liver injury. Acute ER stress led to the accumulation and activation of hepatic macrophages, which preceded hepatocyte apoptosis. Notably, macrophage depletion mitigated liver injury induced by ER stress, underscoring their detrimental role. Mechanistic studies revealed that ER stress stimulates macrophages predominantly via the PERK signaling pathway, regardless of its canonical substrate ATF4. hnRNPA1 has been identified as a crucial mediator of PERK-driven macrophage activation, as the overexpression of hnRNPA1 effectively reduced ER stress and suppressed pro-inflammatory activation. We observed that hnRNPA1 interacts with mRNAs that encode UPR-related proteins, indicating its role in the regulation of ER stress response in macrophages. These findings illuminate the cell type-specific responses to ER stress and the significance of hepatic macrophages in ER stress-induced liver injury. Collectively, the PERK-hnRNPA1 axis has been discovered as a molecular mechanism for macrophage activation, presenting prospective therapeutic targets for inflammatory hepatic diseases such as acute liver injury.

• Journal of Environmental Health Sciences
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• v.23 no.2
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• pp.83-88
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• 1997

To evaluate the effect of bromobenzene pretreatment on the bromobenzene metabolism, the animal group was induced the stage of slight liver damage with 7 times bromobenzene injection every two days (400 mg/kg body wt. i.p.). In the present experimental animal model, the single dose of bromobenzene(400 mg/kg body wt. i.p.) was injected to the bromobenzene-pretreated rats and the hepatic aniline hydroxylase(AH) activity, glutathione(GSH) content and glutathione S-transferase (GST) activity were determined at the intervals of 2, 4, 8, 24 hours throughout 24 hr. The activities of hepatic AH and GST were generally higher in bromobenzene-pretreated rats than those in normal group throughout the whole course of experiment. Furthermore, the decreasing rate of hepatic GSH content was also higher in bromobenzene pretreated rats than in normal rats. Moreover, the value of V$_{max}$ in hepatic GST was higher in bromobenzene pretreated rats than that in the normal rats. In conclusion, these results indicate that the pretreatment of bromobenzene may rather enhance the bromobenzene metabolism.

• Korean Journal of Clinical Pharmacy
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• v.3 no.2
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• pp.163-168
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• 1993

The influence of cimetidine pretreatment(100mg/kg, single i.p.) on the hepatic blood flow was investigated using pharmacokinetic parameters of indocyanine green(ICG) in the rat on the basis of hepacc perfusion-limited model. ICG(1mg/kg) was respectively administered via femoral and portal vein to the control and to the cimetidine-pretreated rats. The rate constant K12, K20 and the systemic clearance(CLt) of ICG were significantly(p<0.05) decreased ill the cimetidine-pretrea-to(B rats, but no significant diffirences were observed in hematocrit and liver weight. The biliary excretion rates of ICG were also decreased regardless of the route of administration in the cimetidine-pretreated rats. And also the hepatic blood flow in rats was decreased about $16\%$ by cimetidine. It may be concluded that the decreased hepatic blood flow with cimetidine mainly contributed to the decreased hepatic uptake and the decreased systemic clearance of ICG.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.1
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• pp.40-45
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• 1991

The release of hepatic triglyceride lipase from cultured rat hepatocytes and its hormonal regulation were studied. The activity of lipase released into the medium in the presence of heparin was increasing during 24 hours on the 2nd of culture while this was 10% in the absence of heparin as compared with the lipase activity in the presense of heparin. When hepatocytes were cultured with anti-hepatic triglyceride lipase lgG the lipase activity was supp-ressed by 92% The results suggest that the enzyme relaeased into culture medium is identical to hepatic triglyceride lipase which can be released only in the presence of heparin the model of release being similar to that of lipoprotein lipase from adipocytes. The addition of monensin to the medium resulted in The inhibition of lipase secretion by 61% Insulin enhanced lipase activity only 20% whereas dexamethasone suppressed the activity by 44% These data inidica-ted that hepatic triglyceride lipase is secreted and released from hepatocytes in the presence of heparin and its secretion is regulated by hormones.