• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.9-16
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• 2001

To investigate the effects of safflower seed supplementation diet on the hepatic injury of rats administered with carbon tetrachloride (CCI$_4$), histopathological changes were assessed following acute and chronic administration in rats. In acute cases, all rats in group fed with 10% safflower seed supplementation diet survived despite the administration of lethal doses of $CCl_4$. However, most rats in group fed with control diet died. The hepatic injuries of survived rats, in the histopathological findings, were mild compared to those of dead rats. In the chronic cases, livers of group 2 fed with control diet were more progressive in fatty changes and centrilobular necrosis than those of group 3 fed with 20%safflower seed diet. However, after six weeks, livers of group 2 and 3 showed severe necrosis and mild fibrosis at the same time. Group 5 fed with 10% safflower seed supplementation diet and water containing 0.05% phenobarbital sodium showed mild fatty changes and necrosis compared with group 4 fed with control diet and water containing 0.05% phenobarbital sodium at sixth week. At 8 to 10 wee71s after the administration of $CCl_4$, severe fibrosis. fatty changes and marked necrosis were observed in group 4, but hepatic injuries were less severe in group 5. The present results suggested that safflower seed has some protective effect in hepatic lesions and consequently delay the progression of hepatic fibrosis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1658-1663
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• 2006

Panax notoginseng (Buck) F.H chen. root (PNS) is used as a therapeutic agent to stop haemorrhages and a tonic to promote health in Korean and Chinses medicine. The pharmacokinetic profiles of the main PNS are still not accurately investigated. Our preliminary aim is to elucidate the pharmacokinetics features of the PNS in rats. Objective of this study is to determine whether PNS affects hepatic microvascular dysfunction elicited by gut ischemia and reperfusion (I/R), since gut I/R causes hepatic microvascular dysfunction, and to investigate the role of nitric oxide (NO). No has been found to be a modulator of the adhesive interactions between platelet and endothelial cells. Male Wistar rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor the number of non-perfused sinusoids (NPS). In another set of experiments, PNS (1 g/kg pre day intragastrically) was administered to rats for 7 days. In some experiments, dexamethasone (ST) (2 mg/kg per day intravenously) was administered. In control rats, gut I/R elicited increases in the number of NPS, and plasma TNF-${\alpha}$ and ALT activities, and these changes were mitigated by the pretreatment with PNS. Pretreatment with an No synthase inhibitor diminished the protective effects of PNS on the increase in NPS and plasma TNF-${\alpha}$ levels, but not its effect on the increase in plasma ALT activities. Pretreatment with PNS increased plasma nitrite/nitrate levels. The responses caused by gut I/R were attenuated by the pretreatment with ST. Pretreatment with an NO synthase inhibitor did not affect the effect of ST. These results suggest that PNS attenuates the gut I/R-induced hepatic microvascular dysfunction and inflammatory responses such as TNF-${\alpha}$ production in the early phase via enhancement of NO production, and sequential hepatocellular damage via its anti-inflammatory effect like corticosteroid effect.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.4
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• pp.392-397
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• 1993

The present work was undertaken to investigate the protective mechanism of Oenanthe iavanicu n-butanol extract on the carbon tetrachloride-induced hepatotoxicity in mice. It was observed that a striking enhancement of serum alanine aminotransferase and hepatic lipid peroxide content after carbon tetrachloride administration were markedly decreased by the presentment of Oenanthe javanica extract for 5 days. It was also observed that the hepatic aniline hydroxylase, catalase, glutathione S-transferase activity and glutathione content were not changed by the injection of Oenanthe javanica extract for 5 days. Whereas, hepatic xanthine oxidase activity was inhibited by the treatment of Oenanthe javanica extract for 5 days. After treatment with Oenanthe javanica extract, xanthine oxidase activity was decreased with dose and time-dependent manner as compared to control group. However, hepatic xanthine oxidase activity was not affected by the addition of Oenanthe javanica extract in vitro. These results suggest that the inhibition of hepatic xanthine oxidase activity by the injection of Oenanthe javanica extract is believed to be a possible protective mechanism for the carbon tetrachloride-indured hepatotoxicity in mice.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.750-756
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• 1994

The effect of onion juice on ethanol -induced lipid peroxidation were studied were studied in rats. The contents of thiobarbituric acid (TBA) -reactants increased significantly in liver thanol(4ml/kg/day) administered -rats. The activities of serum alanine aminotransferase and alkaline phosphatase increased by ethanol administration compared with control group, but alterations of antioxidant enzymes activities in liver of ethanol administered rats were not significant vs control group. The glutathione contents in liver decreased by ethanol , whereas the glutathione level increased in ethanol and onion juice group compared with ethanol group. The contents of hepatic TBA-reactants and serum aminotrasnferase activity in ethanol group were reduced by onion juice administration. In these results, increased hepatic TBA-reactants of liver in ethanol group might be due to decreased glutathione contents in liver. Reduced glutathione (GSH) plays an important roles in the liver in several detoxification and the reduction of lipid peroxides. So the protective effects of onion juice on ethanol-induced increment of TBA-reactants may be due to the increament of lgutathions content. The glutathione depletion by ethanol was an important factor of ethanol-induced cell damage, and the prevention of onion juice to the glutathione depletion reduced by ethanol may be an important factor on the protection from ethanol-induced lipid perpxidation in rats.

• Archives of Pharmacal Research
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• v.28 no.12
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• pp.1392-1399
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• 2005

This study evaluated the effect of $\alpha$-tocopherol ($\alpha$-TC), ischemic preconditioning (IPC) or a combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with $\alpha$-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the aminotransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. $\alpha$-TC and IPC individually attenuated these changes. $\alpha$-TC combined with IPC ($\alpha$-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by $\alpha$­TC, IPC, and $\alpha$-TC+IPC. These results suggest that either $\alpha$-TC or IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but $\alpha$- TC combined with IPC offers no significant additional protection.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1025-1034
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• 2009

This study was carried out to examine the protective effect of Cultured Wild Ginseng(CWG) on the acute and subacute toxicities induced by doxorubicin(Doxo) in mice. Heart and liver weight was decreased following Doxo administration. In contrast, such a decrease was significantly attenuated by CWG administration. The value of serum CPK in Doxo group was increased compared with normal group. But the value of CWG group were decreased significantly compared with the values of Doxo group in the liver of the Doxo group, cloudy swelling of hepatic cells and narrowing of sinusoids were observed. Whereas in the CWG group, well oriented hepatic cell cords and sinusoids were observed. In the testis of the Doxo group, necrotic and degenerative changes of the seminiferous tubules, especially beneath testicular membrane were observed. But those lesions were alleviated in CWG group. Cross sectional area of testis and diameter of semineferous tubule were significantly increased in CWG group compared with Doxo group. Body weight was reduced in Doxo group compared with normal group. In contrast, such a decrease was significantly attenuated by CWG administration atwa5th day. Spermatogenetic cells in seminiferous tubules were necrotic and desquamated and the cellularity of seminiferous epithelia was reduced in Doxo group. But those lesions were attenuated by CWG administration. Cross sectional area of testis and diameter of seminiferous tubule were significantly increased in CWG group compared with Doxo group. In addition, the increase in lipid peroxidation(LPO) in testis was inaddition, the, iout such a increased was significantly inhibited in CWG group. BrdU labelled cells in the seminiferous tubules were remarkably decreased in Doxo group. Whereas the number of seminiferous tubules labelled with BrdU in spermatogonia was increased by CWG administration. The obtained results suggest that CWG has protective effect on doxorubicin-induced toxicity. This effect might be mediated through the supplementation of vital energy.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.5
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• pp.569-573
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• 2009

This study was carried out to investigate the protective effect of Hovenia dulcis Thumb leaves extract on liver damage in benzo($\alpha$)pyrene (B($\alpha$)P)-treated mice. Hovenia dulcis Thumb leaves methanol extract was intra-peritoneally injected once daily for 5 successive days, followed by treatment with B($\alpha$)p. The elevated activities of serum aminotransferase and hepatic cytochrome P450 by B($\alpha$)p were decreased by pretreatment with Hovenia dulcis Thumb leaves extract. Hovenia dulcis Thumb leaves extract also significantly prevented the elevation of hepatic malondialdehyde content and depletion of glutathione content induced by B($\alpha$)P. In addition, the increased activities of superoxide dismutase, catalase and glutathione peroxidase after B($\alpha$)P-treatment were decreased. On the other hand, glutathione S-transferase activity was increased by pretreatment with Hovenia dulcis Thumb leaves extract. These results suggest that Hovenia dulcis Thumb leaves extract have a protective effect on liver damage by B($\alpha$)P through the mechanisms of decreasing lipid peroxide and activities of free radical generating enzymes.

• Nutritional Sciences
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• v.6 no.3
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• pp.141-147
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• 2003

Fruits and vegetables reportedly have a protective effect against hyperlipidemia and oxidative disease. Accordingly, this study aimed to investigate the lipid-lowering effect and antioxidative capacity of persimmon leaf extract (PLE) in rats fed a high-cholesterol diet. Male rats were fed a high-cholesterol (1% wt/wt) or high-cholesterol diet supplemented with Lovastatin (0.02% wt/wt) or PLE (0.2% wt/wt) for 5 weeks. The concentration of plasma total cholesterol was significantly lower in the PLE group than in the lovastatin group. However, the concentration of plasma HDL-cholesterol and the ratio of HDL-cholesterol/total-cholesterol (%) were significantly higher in the PLE group than in the control group. The PLE supplement also significantly lowered the contents of hepatic cholesterol and triglyceride. In comparing fecal sterol contents, the PLE group saw a significant increase of both neutral and acidic sterol compared to the other groups. The PLE supplement significantly lowered plasma GOT and GPT activity, which ave indices of hepatic toxicity. Plasma TBARS concentration was significantly lower in the PLE group than in the control group, while hepatic TBARS level was not significantly different between the groups. In a comparison of hepatic antioxidant parameters, SOD, catalase and GSH-Px activity were significantly higher in the PLE group than in the control group. However, the PLE supplement significantly towered antioxidant enzyme activity in the erythrocyte. Furthermore, these results suggest that supplementation of PLE promoted the excretion of fecal sterols, thereby leading to decreased absorption of dietary cholesterol. In addition, PLE may play an important role in regulating antioxidative capacities by altering SOD and ChT activity.

• The Journal of Dong Guk Oriental Medicine
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• v.6 no.1
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• pp.91-106
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• 1997

The purpose of this study is to observe tile protective effect of Leeganpunsusan on serum reaction and hepatic tissue in galactosamine treated rats. In this study, the experimental rats divided three group(Normal, Control and sample group). Under the same condition, normal and control groups were administered water, sample group was administered Leeganpunsusan for 15 days. The last day, both normal and control goups were injected to abdomen with galactosamine. The rates of lipid peroxide, SOD(activity) and xanthine oxidase(activity) were measured. The results were obtained as follows : Effects of the extract of Leeganpnnsusan on the hepatic lipid peroxidation, xanthine oxidase activity in VITRO, as compared with control group were significantly decreased with the level of concentration of extract prepared from Leeganpunsusan. In VIVO, the hepatic content of lipid peroxide, the rate of type changing(type D to O) and xanthine oxidase activity were significantly decreased in galactosamine-treated rats. Effect of on the hepatic cytosolic superoxide dismutase activity was significantly increased.

• Toxicological Research
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• v.34 no.1
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• pp.23-29
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• 2018

Ethanol-induced fat accumulation, the earliest and most common response of the liver to ethanol exposure, may be involved in the pathogenesis of liver diseases. Isoliquiritigenin (ISL), an important constituent of Glycyrrhizae Radix, is a chalcone derivative that exhibits antioxidant, anti-inflammatory, and phytoestrogenic activities. However, the effect of ISL treatment on lipid accumulation in hepatocytes and alcoholic hepatitis remains unclear. Therefore, we evaluated the effect and underlying mechanism of ISL on ethanol-induced hepatic steatosis by treating AML-12 cells with 200 mM ethanol and/or ISL ($0{\sim}50{\mu}M$) for 72 hr. Lipid accumulation was assayed by oil red O staining, and the expression of sirtuin1 (SIRT1), sterol regulatory element-binding protein-1c (SREBP-1c), AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor alpha ($PPAR{\alpha}$) was studied by western blotting. Our results indicated that ISL treatment upregulated SIRT1 expression and downregulated SREBP-1c expression in ethanol-treated cells. Similarly, oil red O staining revealed a decrease in ethanol-induced fat accumulation upon co-treatment of ethanol-treated cells with 10, 20, and $50{\mu}M$ of ISL. These findings suggest that ISL can reduce ethanol induced-hepatic lipogenesis by activating the SIRT1-AMPK pathway and thus improve lipid metabolism in alcoholic fatty livers.