• 약학회지
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• 제56권4호
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• pp.260-267
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• 2012

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellaria baicalensis, on hepatic injury caused by ischemia/reperfusion (I/R) in alcoholic fatty liver. Rats were fed an ethanol liquid diet or a control isocaloric diet for 5 weeks, and then subjected to 60 min of hepatic ischemia and 5 h of reperfusion. Baicalin (200 mg/kg) was administered intraperitoneally 24 and 1 h before ischemia. After reperfusion, baicalin attenuated the increase in serum alanine aminotransferase activity. The levels of cytosolic cytochrome c protein expression, caspase-3 activity, the number of apoptotic cells increased after reperfusion, which were higher in ethanol-fed animals, were attenuated by baicalin. Following I/R, the hepatic lipid peroxidation was elevated, whereas hepatic glutathione content was decreased. These changes attenuated by baicalin. In ethanol-fed animals, baicalin augmented the increases in heme oxygenase-1 protein and mRNA expressions, and nuclear Nrf2 expression. In conclusion, our findings suggest that baicalin ameliorates I/R-induced hepatocellular damage by suppressing apoptosis and oxidative stress in alcoholic fatty liver.

• 한국독성학회:학술대회논문집
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• 한국독성학회 1998년도 국제심포지움 및 추계학술대회
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• pp.54-54
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• 1998

• 대한본초학회지
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• 제26권3호
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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.

• 한국환경보건학회지
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• 제19권2호
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• pp.69-77
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• 1993

In the present study, the comparison of liver damage in carbon tetrachloride (CCl$_4$)-treated rats with that those pretreated with ethanol and an effect of liver injury on the serum and liver xanthine oxidase (XOD) activity were evaluated. The increasing rate of liver weight per body wt., the levels of serum alanine aminotransferase, and the decreasing rate of hepatic glucose-6-phosphatase activity and the protein contents in the liver cell were higher in carbon tetrachloride-treated animals pretreated with ethanol than the carbon tetrachloride-treated group. Especially, the histopathological findings also showed more severe liver damage in the ethanol-pretreated rats than the rats treated with carbon tetrachloride only. In such a experimental condition the xanthine oxidase activity of serum and liver both of carbon tetrachloride-treated rats and those pretreated with ethanol were higher than that of each control group. And the increasing rate of xanthine oxidase enzyme activity to the control group was higher in carbon tetrachloride-treated group pretreated with ethanol than those treated with CCl$_4$. In addition, the heptic uricase activity and the serum levels of uric acid were more increased in carbon tetrachloride-treated group pretreated with ethanol than those in the CCl$_4$-treated rats. On the other hand, there were no statistical differences in hepatic catalase and glutathione S-transferase activities between the CCl$_4$-treated rats and those pretreated with ethanol. In conclusion, it is assumed that the more severe liver damage in ethanol pretreated rats would be due to oxygen free radical produced by the xanthine oxidase system.

• Biomolecules & Therapeutics
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• 제10권1호
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• pp.12-18
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• 2002

Silymarin and curcumin have been used for supportive treatment of liver disease of difffrent etiology due to their hepatoprotective activities. The present study was carried out to investigate the hepatoprotective efffcts of silymarin and/or curcuma extract against hepatotoxins induced liver injury. To investigate hepatoprotective effects, the silymarin and/or curcuma extract were pre-treated orally to experimental animals. And thereafter a single dose of hepatotoxin, carbon tetrachloride ($CCl_4$) and acetaminophen were administered through oral or intraperitoneal route, respectively. Chronic liver damage was induced by subcutaneous injection of $CCl_4$ for 3 weeks (2 times/week). Hepatoprotective and therapeutic effects were monitored by estimating serurn ALT and AST levels and by measuring hepatic glutathione (GSH) and malondialdehyde (MDA)levels. Collagen type 1 was detected with irnrnunostaining to assess fibrosis. The results showed that the mix-ture of silymarin and curcuma extract significantly reduced serum biochemistry levels and MDA levels com-pared with those of control group in both acute and chronic animal models. In antifibrotic effect, the relative hepatic collagen content was significantly decreased by silymarin and/or curcuma extract treatment. It was concluded that the complex of silymarin and curcuma extract have a both hepatoprotective and therapeutic effect synergically in rat liver injury induced by heptotoxins.

• 한국식품위생안전성학회지
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• 제14권1호
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• pp.60-66
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• 1999

Diethylnitrosamine (DEN) is known as a potential hepatic carcinogen by single administration. This study was designed to measure the effects of DEN-induced cell damage on the triglyceride and cholesterol concentration in the liver, excluding dietary effects. Fertilized chicken eggs, 10 days before hatching, were randomly divided into three groups (n=20) and each egg was injected 10 ${mu}ell$ of corn oil (vehicle control), 5 $\mu\textrm{g}$ of DEN/10 ${mu}ell$ of DEN/10 ${mu}ell$ into yolk via air sac. After 48 hr and 96 hr incubation, the damage of the chick-embryo liver cell was investigated by electron microscopy and by measuring the concentration of lipid components (total cholesterol, free cholesterol, phospholipid and triglyceride). For eggs administered 10 $\mu\textrm{g}$ of DEN and incuvated 96 hr, in hepatocyte, the nucleus membrane was roughed, the size of nucleolus was apparently increased and euchromatin was accumulated. Mitochondria were condensed and cristae, located mitochondiral inner membrane, were obscured. Additionally, the leaves of triglyceride and cholesterol classes were significantly increased depend on the amount treated with 10 $\mu\textrm{g}$ DEN at 96 hr, but phospholipids component of cell membrane, were decreased with significance. As a conclusion, carcinogen induced hepatic lesion was correlated with the changes in lipid component of liver.

• 한국식품영양과학회지
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• 제15권3호
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• pp.229-234
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• 1986

화분립(花粉粒)의 chloroform으로 인한 간(肝) 및 위장조직(胃臟組織)에 미치는 영향을 알기 위해 rat에 농도별로 chloroform을 투여하고 또 이들과 화분립(花粉粒)을 함께 투여(投與)한 결과, chloroform 농도가 증가할 수록 조직파괴 및 지방변성이 심했으며, 화분립(花粉粒)을 함께 투여(投與)함으로 조직파괴 정도가 약화됨을 알 수 있었고, 화분립(花粉粒)과 함께 투여(投與)하는 chloroform의 농도가 낮을수록 대조군(對照群)의 조직(組織)에 가까운 형태로 회복됨을 볼 수 있었다.

• Journal of Microbiology and Biotechnology
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• 제34권6호
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• pp.1328-1339
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• 2024

Cadmium (Cd) is a prevalent environmental contaminant that poses a potential hazard to the health of both humans and animals. In this study, biosynthesized selenium-enriched Lactobacillus plantarum and selenium nanoparticles (SeNPs) were developed and evaluated for their protective effects against Cd-induced hepatic injury in mice through oral administration for 4 weeks. Cadmium exposure resulted in severe impairment of liver function, as evidenced by increased levels of serum markers of liver injury and, oxidative stress and significant damage to liver tissue, and a notable decrease in the diversity of the intestinal microbiota. Oral administration of Se-enriched L. plantarum (LS) reduced cadmium accumulation in the liver by 49.5% and, restored other cadmium-induced damage markers to normal levels. A comparison of the effects with those of L. plantarum (L) and SeNPs isolated from LS revealed that LS could more effectively alleviate hepatic oxidative stress and reduce the intrahepatic inflammatory responses of the liver, further protecting against cadmium-induced liver injury. These findings suggest that the development of LS may be effective at protecting the liver and intestinal tract from cadmium-induced damage.

• Food Science and Biotechnology
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• 제14권4호
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• pp.558-560
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• 2005

Hepatoprotective effects of white ginseng extract (WGE), and IH-901 (20-O-${\beta}$-D-glucopyranosyl-20(S)-protopanaxadiol) derived from intestinal metabolite of ginsenoside $Rb_1$ were studied using two experimental animal models with chemical-induced hepatic damage. Administration of WGE (200 and 500 mg/kg) and IH-901 (0.01, 0.05, and 0.1 mM/kg) significantly decreased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in acute hepatitic mice induced by $CCl_4$. Administration of WGE (l00 mg/kg) and IH-901 (0.02, 0.04, and 0.08 mM/kg) significantly decreased AST and ALT levels in acute hepatitic rats induced by D-galactosamine. AST and ALT levels of IH-901 groups decreased. These results suggested WGE and IH-901 may have protective effects against chemical-induced hepatic damage.

• Journal of Korean Biological Nursing Science
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• 제2권1호
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• pp.49-63
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• 2000

Aflatoxin $B_1(AFB_1)$ is a potent hepatotoxic and hepatocarcinogenic mycotoxin in human beings. It is accumulated in animal tissues and injured cell through variable metabolic pathway. This study was conducted to determine the effect of antioxidant vitamins on liver function enzymes and hepatic damage of $AFB_1$ treated mice. The 6 weeks old male ICR mice were randomly separated 6 groups, vehicle solvent or vitamin C(10 mg/kg/day) and vitamin E(63.8 mg/kg/day) were administered by intraperitoneal(i.p.) injection and 1 hr later, vehicle solution(DMSO) or $AFB_1$(0.4 mg/kg) were injected. The results obtained as follow ; The levels of liver function enzymes such as GOT, GPT, LDH, and alkaline phosphatase, in sera of mice were remarkably elevated by treatment with $AFB_1$ only. However, those enzymes were significantly alleviated by co-treatment with antioxidant vitamins(p<0.01). Especially the levels of LDH and ALK phosphatase were similar to those of control groups(p<0.01). The transmission electron microscopy(TEM) image of intracellular microrganelles on the liver cell of mice was also degenerated extremely by treatment with $AFB_1$, but vitamin C and vitamin E gave good effects on cellular deformation. The intracellular microrganelles such as mitochondria, endoplasmic reticulum, nucleus and nucleic membrane were nearly disappeared the cellular deformation by antioxidant vitamins co-administration. With above results, we could estimated that antioxidant vitamins blocked AFB1 induced hepatic cell damage.