• Asian-Australasian Journal of Animal Sciences
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• v.27 no.6
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• pp.907-915
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• 2014

Alpha-lipoic acid (${\alpha}$-LA) is not only involved in energy metabolism, but is also a powerful antioxidant that can protect against hepatic oxidative stress induced by some drugs, toxins, or under various physiological and pathophysiological conditions. Here, we investigated the effect of ${\alpha}$-LA against liver oxidative damage in broilers exposed to aflatoxin $B_1$ ($AFB_1$). Birds were randomly divided into four groups and assigned different diets: basal diet, 300 mg/kg ${\alpha}$-LA supplementation in basal diet, diet containing 74 ${\mu}g/kg$ $AFB_1$, and 300 mg/kg ${\alpha}$-LA supplementation in diet containing 74 ${\mu}g/kg$ $AFB_1$, for 3 weeks. The results revealed that the addition of 300 mg/kg ${\alpha}$-LA protected against the liver function damage of broilers induced by chronic low dose of $AFB_1$ as estimated by a significant (p<0.05) change in levels of plasma total protein, albumin, alkaline phosphatase and the activities of liver glutamic-oxalacetic transaminase and glutamic-pyruvic transaminase. The histopathological analysis also showed that liver tissues were injured in the $AFB_1$ diet, but this effect was alleviated by the addition of 300 mg/kg ${\alpha}$-LA. Additionally, $AFB_1$ induced a profound elevation of oxidative stress in birds, as indicated by an increase in malondialdehyde level, a decrease in glutathione peroxidase activity and a depletion of the glutathione content in the liver. All of these negative effects were inhibited by treatment with ${\alpha}$-LA. Our results suggest that the inhibition of $AFB_1$-induced excess production of lipid peroxides and the maintenance of intracellular antioxidant status may play important roles in the protective effects of ${\alpha}$-LA against $AFB_1$-induced oxidative damage in the liver.

• The Journal of Korean Medicine
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• v.37 no.2
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• pp.76-84
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• 2016

Objectives: We evaluated the anti-fatigue effects of Rh2-enriched Korean ginseng (Ginseng Rh2+) using a forced exercise-induced chronic fatigue mouse model. Methods: ICR male mice were subjected to running wheel for 1 h, 5 days/week during 4 weeks, and running velocity was gradually increased. Each running session was followed by oral administration of distilled water, Ginseng Rh2+ (150 or 300 mg/kg), or N-acetyl-L-cysteine (NAC, 100 mg/kg) 1 h later. The exercise tolerance and forced swimming test were performed to evaluate the fatigue condition. Results: Chronic forced exercise reduced the physical activity, as evidenced by the behavioral tests, which were notably ameliorated by Ginseng Rh2+ treatment. Ginseng Rh2+ treatment also attenuated the alterations of energy metabolism and oxidative stress in skeletal muscle tissues and/or sera, including malondialdehyde (MDA), lactate concentration and its related factors (lactate dehydrogenase, blood urea nitrogen, and glucose levels). Conclusion: These findings strongly suggest that Ginseng Rh2+ exerts a potent anti-fatigue effect through modulation of energy metabolism and oxidative response.

• Journal of Life Science
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• v.17 no.11
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• pp.1571-1575
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• 2007

This research was carried out to investigate the effects of Hambag mushroom on the oxidative stress in diabetic rats, Sprague-Dawley. The diabetic rats induced by streptozotocin were fed with hambag mushroom-powder(G. frondosa) for 6 weeks. For the level of oxidative stress in liver and pancreas tissues, it was studied by measuring LPO (lipid oxide) level as an indicator of lipid peroxidation, XOD(xanthine oxidase) as one of important sources for free radicals and the levels of GSH and GST as anti-oxidant systems. Also, as an indicator of liver damaged by oxidative stress, the activities of serum ALT and AST were measured. It was observed that the levels of ALT, AST, LPO and XOD were higher by about two times in both tissues from diabetic rats than in those from control rats. This indicates that the oxidative stress induced by diabetes caused the tissues damages. However, these levels were decreased in the tissues from rats with hambag mushroom-powder. Futhermore, the activity of GST were higher in both tissues from diabetic rats fed with hambag mushroom-powder than in those from diabetic rats. Thus, it is considered that the hambag mushroom-powder decreases the level of oxidative stress by increasing activity of anti-oxidant system such as GSH and GST. It is suggested that the hambag mushroom-powder can be useful for preventing the tissues damaged by diabetes-induced oxidative stress.

• Herbal Formula Science
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• v.30 no.3
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• pp.155-163
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• 2022

Objectives : Lonicera japonica is known for anti-inflammation and antibiotic effect in Korean medicine. This study aimed for investigating the cytoprotective effect of Lonicera japonica extract (LJE) for HepG2 cells against arachidonic acid (AA)+iron-induced oxidative stress. Methods : The effect of LJE on cell viability was assessed by MTT assay. ROS assay was selected to assess antioxidant effect of LJE. To assess LJE's effect on mitochondrial function, flow cytometric analysis was operated. And immunoblot analysis was used to establish the underlying mechanism of LJE. Results : LJE protected HepG2 cells against AA+iron-induced oxidative stress by phosphorylation of liver kinase B1 and blocked the decline of procaspase 3. Also, LJE preserved the mitochondrial membrane permeability induced by AA+iron. Conclusion : LJE protected the hepatocyte from AA+iron-induced oxidative stress by activation of LKB1 by the preservation of mitochondrial functions.

• Herbal Formula Science
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• v.31 no.1
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• pp.41-51
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• 2023

Objectives : Raphani Semen (Raphanus sativus L.) is known for the various beneficial effects in Korean medicine. This study aimed to investigate the effect of Raphani Semen extract (RSE) against arachidonic acid (AA)+iron-induced oxidative stress in cells. Methods : Ingredients, their target information, oxidative stress liver injury-related proteins was obtained from various network pharmacology databases and software. A hypergeometric test and enrichment analysis were conducted to evaluate associations between protein targets of RSE. The cell viability was assessed by MTT assay, and immunoblot analysis was used to confirm the molecular mechanisms. Results : A compound-target network of RSE was constructed, which consisted of 336 edges between 18 ingredients and 123 protein targets. PI3K-Akt signaling pathway, ErbB signaling pathway, HIF-1 signaling pathway, PPAR signaling pathway, and AMPK signaling pathway was significantly associated with protein targets of RSE. RSE protected HepG2 cells against AA+iron-induced oxidative stress as mediated with AMPK signaling. Conclusion : RSE was found to protect the cells against oxidative stress via the AMPK signaling pathway.

• Journal of Environmental Health Sciences
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• v.34 no.1
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• pp.49-54
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• 2008

The induction of heme oxygenase-1(HO-1) by UV radiation provides a protective defence against oxidative stress, and has been well demonstrated in skin irradiated with UVA, but not UVB. In this study, we show that the induction of cutaneous HO-l can be attributed to UVB radiation. The expression of HO-1 mRNA was assessed in vivo by reverse transcription-polymerase chain reaction (RT-PCR) analysis, and HO-1 enzyme activity was measured in microsomal preparation from irradiated mice. The mRNA level of HO-1 increases in liver and skin from 1d to 3d after UVB $(3KJ/m^2)$ exposure. The results of gene expression were same pattern of HO-1 enzyme activity in skin, but not in liver. HO-1 mRNA in liver resulted in a progressive increase to 4d after UVB exposure, but HO-1 activity in liver increased to 2d. This finding indicates that UVB radiation is an important inducer of HO-1 and increases in HO activity may protect tissue directly or indirectly from oxidative stress.

• YAKHAK HOEJI
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• v.53 no.6
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• pp.314-320
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• 2009

We examined metabolic conversion of cysteine into glutathione (GSH) and taurine in rat liver under oxidative stress. Administration of tert-butylhydroperoxide (t-BHP) into the portal vein of male rats resulted in a rapid elevation of serum sorbitol dehydrogenase, alanine aminotransferase, and aspartate aminotransferase activities, which decreased gradually in 24 hr. Hepatic cysteine concentration was reduced in 3 hr, and recovered progressively, reaching a level greater than 200% of the normal value in 24 hr. GSH was increased both in liver and blood at 9 hr after t-BHP challenge, whereas hypotaurine or taurine was not altered. $\gamma$-Glutamylcysteine synthetase (GCS) activity was increased from 9 hr after t-BHP treatment, but protein expression of the GCS-heavy subunit was not changed in liver. Activity or expression of cysteine dioxygenase was not affected by t-BHP treatment. Taken together, these data show that an acute oxidant challenge to the rats may induce upregulation of cysteine availability and GCS activity, resulting in an enhancement of hepatic GSH synthesis, but the increased cysteine level does not stimulate taurine synthesis via cysteine sulfinate pathway. It is indicated that the regulation of GSH and taurine biosynthesis from cysteine is not solely dependent on the cysteine concentration in rat liver under oxidative stress.

• Korean Journal of Food Science and Technology
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• v.53 no.5
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• pp.535-543
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• 2021

Particulate matter (PM) causes oxidative stress and can rapidly diffuse from the lung to the blood and accumulate in the liver when inhaled. Natural antioxidants can be used to protect against oxidative stress caused by PM. Sargassum horneri, a brown seaweed, possesses antioxidative activity and is a good source of functional foods. Therefore, this study investigated the antioxidant potential of S. horneri extract (SHE) in the livers of PM-induced asthmatic mice. PM inhalation triggered lipid peroxidation and oxidative stress, and SHE treatment attenuated malondialdehyde in the liver of mice with PM-induced asthma. Furthermore, SHE mitigated the increase in catalase activity. Importantly, SHE reduced the activity of 8-oxoguanine glycosylase (OGG1), a DNA repair enzyme. These results suggest that SHE has antioxidant potential for moderating PM-induced oxidative stress and DNA damage in the liver of asthmatic mice.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.487-496
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• 2011

Objectives : The aim of this study was to investigate the hepatoprotective effect of Soshiho-tang (SSH) in mouse primary liver cells against hydrogen peroxide ($H_2O_2$)-induced oxidative stress. We also elucidated the molecular mechanism of hepatoprotective effect by SSH. Methods : Cell viability, level of ALT, AST and LDH, intracellular ROS level, mRNA expression and activity of antioxidant enzymes were used to evaluate hepatoprotection of SSH against $H_2O_2$. Target gene expressions were analyzed by real-time PCR. Results : Pre-treatment with SSH for 1 hour prevented cytotoxicity against $H_2O_2$. $H_2O_2$-induced ROS level decreased under SSH pre-treatment. mRNA expression of GPx and SOD increased in SSH-treated cells. In addition, HSP72 and HSP40 gene expression were elevated under SSH-treatment. Conclusions : These results indicate that SSH protects mouse primary liver cells from $H_2O_2$-induced oxidative injury. This hepatoprotective activity of SSH is mediated by decreasing intracellular ROS and increasing antioxidant enzyme expression (GPx and SOD) and stress response protein (HSP72 and HSP40).

• The Korea Journal of Herbology
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• v.31 no.1
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• pp.33-40
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• 2016

Objectives : Liver is one of the largest organs in the human, and has a function of detoxification and energy sensing to prevent severe disease. Paeoniae radix has been used to treat a variety of liver diseases such as hepatitis and chronic hepatic failure. Although P. radix has been used as an medicinal herb for a long time, the effects of P. radix on severe oxidative stress and its action mechanism on the liver was not clearly verified.Methods : This study investigated the protective effects of P. radix extract (PRE), and the underlying mechanism of its action in the liver. tert-butyl hydroperoxide (t-BHP) and carbon tetrachlroride (CCl₄) were used to induce oxidative stress in the HepG2 hepatocyte cell line and Sprague-Dawley rats, respectively.Results : t-BHP significantly induced cell death and ROS production in HepG2 cell, as indicated by MTT and FACS analysis. However, pretreatment of PRE inhibited a decrease in cell viability and H₂O₂ production in the HepG2 cells. PRE also blocked the ability of t-BHP to damage in mitochondrial membrane transition. More importantly, PRE induced Nrf2 activation and antioxidant Phase II enzyme, which may have a role in the effects of PRE. In mice, PRE inhibited the liver damage induced by CCl₄.Conclusions : PRE inhibited oxidative stress and hepatic damages as mediated with Nrf2 activation. This study unveil, in part, the effect and mechanism of old medicinal herb, P. radix.