• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2563-2569
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• 2012

Oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Hence there is a great demand for the development of agents with potent antioxidant effect. The aim of the present investigation is to evaluate the efficacy of Moringa oleifera as a hepatoprotective and an antioxidant against 7, 12-dimethylbenz[a]anthracene induced hepatocellular damage. Single oral administration of DMBA (15 mg/kg) to mice resulted in significantly (p<0.001) depleted levels of xenobiotic enzymes like, cytochrome P450 and b5. DMBA induced oxidative stress was confirmed by decreased levels of reduced glutathione (GSH) and glutathione-S-transferase (GST) in the liver tissue. The status of hepatic aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) which is indicative of hepatocellular damage were also found to be decreased in DMBA administered mice. Pretreatment with the Moringa oleifera (200 and 400 mg/kg) orally for 14 days significantly reversed the DMBA induced alterations in the liver tissue and offered almost complete protection. The results from the present study indicate that Moringa oleifera exhibits good hepatoprotective and antioxidant potential against DMBA induced hepatocellular damage in mice that might be due to decreased free radical generation.

• BMB Reports
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• v.39 no.5
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• pp.479-491
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• 2006

Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-${\kappa}B$) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.

• Journal of the Korea Society of Computer and Information
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• v.21 no.7
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• pp.61-66
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• 2016

The frequency of obesity has risen dramatically in recent years but only few safe and effective drugs are currently available. In addition, obesity can induce type 2 diabetes (T2DM), hyperlipidemia and fatty liver disease. Recently, protective effect of purslane extract (PE) on obesity has been reported, but little is known about the role and mechanism of PE in obesity. This study aimed to evaluate the effect of PE on obesity and diabetes in obese mice. In addition, the effect of PE was compared with anti-obesity and diabetes drugs. High-fat diet (HFD)-induced obese mice were treated for 8 weeks with drugs as follows: PE, orlistat, metformin, voglibose or pioglitazone. While PE mixed with normal diet did not have any effects on BW in non-obese mice, PE mixed with HFD significantly reduced BW gain, insulin resistance, and glucose intolerance, without affecting food intake and appetite in obese mice. The effect was comparable to the effects of anti-obesity and diabetes drugs. Furthermore, PE significantly increased the activity of hepatocellular anti-oxidant enzymes, leading to protection of liver from oxidative stress in obese mice. These results suggest that PE treatment may be a useful tool for preventing obesity and complication of obesity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.1
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• pp.199-204
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• 1999

This study has attempted to examine the effect of Artemisia iwayomogi extract on antioxidant and liver function related enzymes in rats fed high fat diet along with B( )P administration. The activities of the serum glutamic oxaloacetic transaminase, glutamic pyruvate transaminase and alkaline phosphatase of the rats fed Artemisia iwayomogi ethanol extract were decreased compared to the control. Similarily, the activities of the enzymes were also decreased when the combination of B( )P and ethanol extracts were administered compared to the group adminstered only B( )P. On the other hand, high fat diet increased the above liver function related enzymes. The activities of antioxidant enzymes including GST, catalase and Cu,Zn SOD were significantly increased by feeding the extracts (p<0.01) in addition to the increase of tocopherol contents in the serum. These results suggest that Artemisia iwayomogi extracts can protect cell membranes from the damages by free radicals or hydroperoxides and further may lead to the protection from cancer risks.

• The Korean Journal of Food And Nutrition
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• v.32 no.5
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• pp.417-424
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• 2019

The purpose of this study was to observe the effects of the polysaccharide (GLP) obtained from the liquid cultured Ganoderma lucidum on the lipidperoxidation in a rat liver microsome and hepatotoxicity in the primary cultured rat hepatocytes. It is well known that the polysaccharide of Ganoderma lucidum exhibits hepatoprotective activity, antitumor activity etc., which many suggest a relationship to lipidperoxidation. The effect of GLP on $CCl_4-$ and galactosamineintoxicated cytotoxicity in the primary cultured rat hepatocytes were reduced the GPT value. In order to the estimate the effects of anti-lipidperoxidation of the polysaccharide, enzymatic and nonenzymatic reaction assays were performed, in vitro, in the rat liver microsome. An enzymatic lipidperoxidation reaction by $ADP+FeCl_3+NADPH$ and $CCl_4+NADPH$, GLP (1 mg/mL) inhibited 77.4% and 39.4%, respectively, and the nonenzymatic reaction displayed a 97.4% strongly inhibition. In the enzymatic and nonenzymatic inducers treated with GLP, the formation of malondialdehyde (MDA) progressively decreased by raising the GLP concentration. These results suggest that the anti-lipidperoxidation and radical scavenging activity of GLP may play an important part in the liver protection action.

• The Journal of Korean Medicine
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• v.24 no.1
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• pp.190-201
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• 2003

Object : This study was designed to investigate the effects of Chungganhaeju-tang (Qingganjiejiu-tang) on cytotoxicity, growth inhibition, apoptosis and expression of cytokine in damaged HepG2 cells. Method : Toxicity on HepG2 cell induced by ethanol and acetaldehyde was measured for viability, cell growth, DNA replication and generation of apoptosis and cytokine. The recovery of the cell activity by Chungganhaeju-tang was estimated for the measured parameters using PCR with different cycle numbers, DNA gel-electrophoresis, and densitometric analysis, Results : Chungganhaeju-tang improves the recovery of HepG2 cells damaged by ethanol or acetaldehyde. The suppressed DNA synthesis of the cell damaged by ethanol or acetaldehyde is improved by Chungganhaeju-tang. A liver-protection effect was shown by the reduction of apoptosis and $TNF-{\alpha},{\;}IL-1{\beta}$ expressions that are induced by ethanol or acetaldehyde. Conclusion : The result indicates that Chungganhaeju-tang reduces toxicity induced by ethanol or acetaldehyde and recovers damaged liver function.

• YAKHAK HOEJI
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• v.53 no.4
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• pp.189-193
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• 2009

To investigate the antioxidant effect of lutein on N-nitrosodimethylamine (NDEA)-induced oxidative stress in mice, we measured lipid peroxidation, superoxide dismutase (SOD) and catalase of various tissues. Body weight was almost similar in lutein and control groups during 3 weeks. NDEA increased significantly the activities of typical marker enzymes of liver function (AST, ALT and ALP) in both groups. However, the increase of plasma aminotransferase activity significantly decreased in lutein group. Lipid peroxidation and SOD in various tissues, such as heart, lung, liver, kidney, spleen and plasma were significantly increased by NDEA, which were significantly reduced by lutein at a dose of 50 mg/kg. Catalase activity decreased significantly in control and lutein groups treated with NDEA, the effect being less in lutein group. Lesser effect on SOD and catalase in NDEA-treated lutein group indicates the improvement of protective mechanisms by lutein. Thus, it can be concluded from the present study that lutein can offer a useful protection against NDEA-induced oxidative stress.

• Toxicological Research
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• v.30 no.4
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• pp.291-296
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• 2014

Saururus chinensis has been reported to contain compounds such as lignans, alkaloids, diterpenes, flavonoids, tannins, steroids, and lipids. Fermentation is commonly used to break down certain undesirable compounds, to induce effective microbial conversion, and to improve the potential nutraceutical values. Previous studies have reported that the fermentation process could modify naturally occurring constituents, including isoflavons, saponins, phytosterols, and phenols, and could enhance biological activities, specifically antioxidant and antimicrobial properties. The probiotic strains used for fermentation exert beneficial effects and are safe. In this study, the antioxidative effects of the Bacillus subtilis fermentation of Saururus chinensis were investigated in a rat model with Triton WR-1339-induced hyperlipidemia by comparing the measured antioxidative biological parameters of fermented Saururus chinensis extract to those of nonfermented Saururus chinensis extract. Fermentation played a more excellent role than nonfermentation in ultimately protecting the body from oxidative stress in the liver of the experimental rats with Triton WR-1339-induced hyperlipidemia.

• IMMUNE NETWORK
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• v.1 no.3
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• pp.213-220
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• 2001

Background: A previous study has shown that Euonymus alatus (EA) has an antidotic activities against inflammation, suggesting possibility that EA can exert this beneficial effects to liver injury by an initial protection against drug-induced hepatocyte demage. The present study was undertaken to evaluate the protective effect of EA-extract on experimentally induced hepatitis in ICR mice and to investigate some mechanisms responsible for its action. Methods: Water EA extract was used in this experiments. The mice received i.p. a dose of 700 mg/kg galactosamine (GalN) together with $5{\mu}g/kg$ of endotoxin (LPS), or received i.v. 12 mg/kg of concanavalin A (Con A). EA (4 mg/mouse) was administrated on day -2, -1 and 0 before induction of liver injury. Liver injury was assessed by measurement of serum alanin amino-transferase (SGPT) levels on 9 hr after GaIN.LPS, or 8 hr after con A administration. Results: Treatment with either GaIN or LPS alone did not cause hepatitis. However, simultaneous administration of GalN and LPS to mice resulted in LPS-dose dependent fulminant hepatitis. GaLN/LPS-induced liver injury was reduced when mice were given EA for 3 days before induction. This preventive effect of Ea was more prominent when EA was given by intraperitoneal route rather then by oral route. Pretreatment of EA or dexamethasone inhibited significantly $TNF{\alpha}$ production in GalL/LPS-injured mice. However, EA-treatment did not influence $TNF{\alpha}$-induced hepatitis in GalN-sensitized mice, suggesting that $TNF{\alpha}$ is likely to act as one of final mediators of endotoxin action and the protective effect of EA might be manifested chiefly by inhibition of endotoxin-induced $TNF{\alpha}$ production, not by blocking the $TNF{\alpha}$-action. Injection of Con A into mice evoked remarkable liver injury in a dose dependent fashion. This liver damage was reduced by EA-pretreatment. Dexamethasone significantly reduced both GalL/LPS-induced and Con A-induced liver damages, showing synergism with EA. However, indomethacin reduced only GalN/ LPS-induced hepatitis, not for Con A-induced hepatitis. Conclusion: These results led to the conclusion that EA may be able to contribute at least in part to prevent the drug-induced hepatotoxicity, and that its anti-hepatitis effects might be manifested directly by modulation of endogenous mediators, such as leukotriese D4, $TNF{\alpha}$ and free radical, and indirectly by regulation of immune mediated responses. Also these results suggested that EA could be developed as a potential antidotic agent.

• Korean Journal of Plant Resources
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• v.30 no.2
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• pp.125-132
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• 2017

Bisphenol A (BPA), a known endocrine disruptor, induces toxicity in cells and in experimental animals. Ginseng extracts were evaluated to determine whether they can inhibit BPA-induced toxicity. The antioxidant activity of fresh ginseng extract (WGE), dried white ginseng extract (DGE), and dried red ginseng extract (RGE) was measured using the DPPH assay. WGE and RGE increased DPPH free radical scavenging activity. Cell viability was measured in HepG2 cells following treatment with BPA and ginseng extracts using the MTT assay. DGE and RGE increased HepG2 cell viability following treatment with $200{\mu}M$ BPA. RGE reduced levels of biochemical markers of liver damage, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) that increased in mice following treatment with BPA. In addition, the regeneration and proliferation of damaged liver cells were significantly increased in RGE-treated mice. Moreover, RGE inhibited hepatic fibrosis in the surrounding area and in the central vein of the liver microstructure. RGE also significantly inhibited BPA-induced cytotoxicity. In addition, RGE protected liver damage and regenerated liver tissues in BPA-treated animals. These results show that RGE may represent a potential candidate drug for the treatment and prevention of liver damage caused by environmental toxins.