• Nutritional Sciences
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• v.6 no.2
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• pp.67-72
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• 2003

This study was conducted to investigate the effect of oligosaccharide on the reduction of oxidative stress. Sprague-Dawley rats were fed an AIN-93G diet or a diet containing 5% soybean oligosaccharide for 6 weeks. Each group was divided into two sub-groups after streptozotocin (STZ) injection and fed the control diet or the diet containing oligosaccharide for the next 12 days. The number of fecal bifidobacteria increased significantly in groups fed oligosaccharide diet. Elevated blood glucose concentration after STZ injection declined faster in the oligosaccharide fed group. Liver thiobarbituric acid reactive substance concentration, as an indicator of oxidative stress, did not increase in groups fed the oligosaccharide diet after the STZ injection. In addition, these groups had significantly higher glutathione peroxidase activity both in the plasma and the liver than groups fed the control diet. The results of this study suggest that soybean oligosaccharide has a beneficial effect in reducing oxidative stress in streptozotocin-injected rats.

• Journal of Sericultural and Entomological Science
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• v.42 no.1
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• pp.58-64
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• 2000

This study was designed to investigate the effects of silk fibroin powder (Mw 500) on oxidative stress and membrane fluidity in liver membranes of rats. Sprague-Dawley (SD) male rats (160$\pm$10g) were fed basic diet (control group), and experimental diets (SEP-2.5 and SFP-5.0 groups) added 2.5 and 5.0 g/kg BW/day for 6 weeks. Cholesterol levels resulted in a significant decrease (12.1% and 9.0%, respectively) in the liver mitochondria and microsomes of SEP-5.0 group compared with control group. Membrane fluidity as significantly increased (16.1% and 16.5%, 5.8% and 17.4%) in the liver mitochondria and microsomes were significantly inhibited (16.1% and 18.3%, 8.1% and 15.1%, respectively) at the SFP-2.5 and SEP-5.0 groups compared with control group. Induced oxygen radicals (BOR) in liver mitochondria and microsomes were significantly inhibited (16.1% and 18.3%, 8.1% and 15.1%, respectively) at the SFP-2.5 and SEP-5.0 groups compared with control group. Induced oxygen radicals (IOR) in liver microsomes were significantly inhibited (17.0% and 26.6%, respectively) at the SFP-2.5 and SFP-5.0 groups compared with control group, but IOR in liver mitochondria was significantly inhibited about 12.3% at the SWP-400 group only compared with control group. Lipid peroxide (LPO) levels were significantly decreased (8.3% and 18.0%, 13.4% and 18.4%, respectively) in the liver mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. Oxidized protein (OP) levels were dose-dependently decreased (5.4% and 11.6%, 19.0% and 24.4%, respaectively) in the iver mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. These results suggest that administration of SFP may play an effective role in attenuating an oxidative stress and increasing a membrane fluidity in liver membranes.

• Molecules and Cells
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• v.42 no.9
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• pp.672-685
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• 2019

Currently, liver transplantation is the only available remedy for patients with end-stage liver disease. Conservation of transplanted liver graft is the most important issue as it directly related to patient survival. Carbonyl reductase 1 (CBR1) protects cells against oxidative stress and cell death by inactivating cellular membrane-derived lipid aldehydes. Ischemia-reperfusion (I/R) injury during living-donor liver transplantation is known to form reactive oxygen species. Thus, the objective of this study was to investigate whether CBR1 transcription might be increased during liver I/R injury and whether such increase might protect liver against I/R injury. Our results revealed that transcription factor Nrf2 could induce CBR1 transcription in liver of mice during I/R. Pre-treatment with sulforaphane, an activator of Nrf2, increased CBR1 expression, decreased liver enzymes such as aspartate aminotransferase and alanine transaminase, and reduced I/R-related pathological changes. Using oxygen-glucose deprivation and recovery model of human normal liver cell line, it was found that oxidative stress markers and lipid peroxidation products were significantly lowered in cells overexpressing CBR1. Conversely, CBR1 knockdown cells expressed elevated levels of oxidative stress proteins compared to the parental cell line. We also observed that Nrf2 and CBR1 were overexpressed during liver transplantation in clinical samples. These results suggest that CBR1 expression during liver I/R injury is regulated by transcription factor Nrf2. In addition, CBR1 can reduce free radicals and prevent lipid peroxidation. Taken together, CBR1 induction might be a therapeutic strategy for relieving liver I/R injury during liver transplantation.

• The Journal of Internal Korean Medicine
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• v.42 no.6
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• pp.1269-1284
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• 2021

Objectives: Phragmitis Rhizoma is the fresh or dried rhizome of Phragmites communis Trin., which has been prescribed in traditional Korean medicine to relieve fever and vomiting and to nourish the body fluids. Recently, the protective effect of Phragmitis Rhizoma extract or its components on myelotoxicity and inflammatory responses have been reported, but no study has yet been conducted on oxidative stress. Methods: The present study investigated whether an ethanol extract of Phragmitis Rhizoma (PR) could protect against cellular damage induced by oxidative stress in Chang liver cells. Results: Pretreatment with PR significantly suppressed the hydrogen peroxide (H₂O₂)-induced reduction of Chang cell viability and generation of reactive oxygen species (ROS), thereby deferring apoptosis. PR also markedly inhibited H₂O₂-induced comet tail formation and phospho-γH2AX expression, suggesting that PR protected against oxidative stress-mediated DNA damage. PR also effectively prevented the inhibition of ATP synthesis in H₂O₂-treated Chang cells by inhibiting the loss of mitochondrial membrane potential, indicating that PR maintains energy metabolism through preservation of mitochondrial function while eliminating ROS generated by H₂O₂. Immunoblotting results indicated that PR attenuated the H₂O₂-induced downregulation of Bcl-2 and upregulation of Bax expression. Conclusions: PR protects against oxidative injury in Chang liver cells by regulating energy homeostasis via ROS generation blockade, which is at least partly mediated through inactivation of the mitochondria-mediated apoptosis pathway.

• The Korea Journal of Herbology
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• v.24 no.3
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• pp.109-119
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• 2009

Objectives : The present study was purposed to compare Adenophorae Radix (henceforth AR), Codonopsis lanceolatae Radix (henceforth ClR) and Glehniae Radix cum Rhizoma (henceforth GRcR) concerning their anti-oxidant effect. Methods : We measured eythrocyte, leukocyte, thrombocyte, serum albumin, total bilirubin, LDL cholesterol, and glucose as well as SOD, GSH, catalase, NO, and MDA in the rat liver oxidatively stressed by AAPH. Results : 1. The oxidative stress-induced thrombocyte levels were significantly decreased in CIR-treated and GRcR-treated groups. 2. The oxidative stress-impaired SOD acitivities were significantly recovered in AR-treated and GRcR-treated groups. 3. The oxidative stress-reduced GSH contents were significantly increased in ClR-treated and GRcR-treated groups. 4. The oxidative stress-reduced catalase contents were significantly increased in all of the three groups. 5. The oxidative stress-induced NO productions were significantly decreased in all of the three groups. Conclusions : AR, ClR, and GRcR altogether showed the anti-oxidant effect in the rat liver oxidatively stressed by AAPH. The anti-oxidant properties of tAR, ClR, and GRcR seem to be similar even if those have different botanical properties and different medical efficacies in oriental medicine.

• The Korea Journal of Herbology
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• v.26 no.3
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• pp.47-56
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• 2011

Objectives : This study investigated whether the water extract of Spatholobi Caulis (SCE) has the ability to protect hepatocyte against oxidative stress induced by tert-butylhydroperoxide (tBHP) in vitro and $CCl_4$ in vivo. Methods : In vitro, HepG2 cells pre-treated with Spatholobi Caulis water extract (1, 3, 10, $30{\mu}g$/ml) for 12h and further incubated with tBHP ($100{\mu}M$) for the next 12h. Cell viability was assessed by MTT assay. In vivo, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE; 50, 100 mg/kg) for 4 days and then, injected with $CCl_4$ 1 mg/kg body weight to induce acute liver damage. Results : Treatment with SCE inhibited cell death induced by tBHP, as evidenced by alterations in the levels of the proteins associated with apoptosis:SCE prevented a decrease in $Bcl_2$, and cleavage of poly(ADP-ribose)polymerase and pro-caspase-3. Moreover, SCE inhibited the ability of tBHP to generate $H_2O_2$ production, thereby restoring GSH content. Moreover, SCE treatments in rats effectively decreased liver injuries induced by a single dose of $CCl_4$, as evidenced by decreases in hepatic degeneration and inflammation as well as plasma alanine aminotransferase and lactate dehydrogenase activities. Consistently, treatments of SCE also protected liver in rats stimulated by $CCl_4$, as indicated by restoration GSH and prevention of MDA in the liver. Conclusions : SCE has the ability 1) to protect hepatocyte against oxidative stress induced by tBHP and 2) to prevent $CCl_4$-inducible acute liver toxicity. Present findings may be informative not only in elucidating the pharmacological mechanism of Spatholobi Caulis, but in determining its potential application for oxidative cellular damage in the liver.

• The Journal of the Society of Korean Medicine Diagnostics
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• v.17 no.3
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• pp.275-286
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• 2013

In the present study, antioxidant activity and protective effect of extracts from Sambucus williamsii var. coreana stems (SWC) were evaluated on tert-butyl hydroperoxide (t-BHP) induced oxidative stress in human liver (Chang) cells. Antioxidant activities of the SWC extracts were determined by various radical scavenging activities, such as DPPH, ferric reducing antioxidant power (FRAP), 2,2'-azinobis-(3-ethybenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity and oxygen radical absorbance capacity (ORAC) assay. SWC extracts showed strong antioxidant effect on various assay. To determine the hepatoprotective effects of SWC on t-BHP induced oxidative damage, cell viability was measured using MTT assay. Pretreatment of SWC extracts showed increasing cell viability, decreasing ROS and restoring mitochondria membrane potential on t-BHP induced oxidative stress in Chang cells. Our findings suggest that SWC extracts may be considered a potential agent for therapeutic protective effect from oxidative stress through its antioxidant activity.

• Nutrition Research and Practice
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• v.5 no.6
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• pp.520-526
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• 2011

Folate deficiency and hyperhomocysteinemia are found in most patients with alcoholic liver disease. Oxidative stress is one of the most important mechanisms contributing to homocysteine (Hcy)-induced tissue injury. However it has not been examined whether exogenous administration of folic acid attenuates oxidative stress and hepatic toxicity. The aim of this study was to investigate the in vivo effect of folic acid supplementation on oxidative stress and hepatic toxicity induced by chronic ethanol consumption. Wistar rats (n = 32) were divided into four groups and fed 0%, 12%, 36% ethanol, or 36% ethanol plus folic acid (10 mg folic acid/L) diets. After 5 weeks, chronic consumption of the 36% ethanol diet significantly increased plasma alanine transaminase (ALT) (P < 0.05) and aspartate transaminase (AST) (P < 0.05), triglycerides (TG) (P < 0.05), Hcy (P < 0.001), and low density lipoprotein conjugated dienes (CD) (P < 0.05) but decreased total radical-trapping antioxidant potential (TRAP) (P < 0.001). These changes were prevented partially by folic acid supplementation. The 12% ethanol diet had no apparent effect on most parameters. Plasma Hcy concentration was well correlated with plasma ALT (r = $0.612^{**}$), AST (r = $0.652^*$), CD (r = $0.495^*$), and TRAP (r = $-0.486^*$). The results indicate that moderately elevated Hcy is associated with increased oxidative stress and liver injury in alcohol-fed rats, and suggests that folic acid supplementation appears to attenuate hepatic toxicity induced by chronic ethanol consumption possibly by decreasing oxidative stress.

• Herbal Formula Science
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• v.31 no.2
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• pp.111-124
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• 2023

Objectives : Oxidative stress is an important cause of many diseases including liver injury. Therefore, adequate regulation of oxidative stress plays a pivotal role in maintaining liver function. Until recently, there has been no studies on the hepatoprotective effect of Samchulgeonbi-tang (SCGBT). Therefore, the hepatoprotective effect of SCGBT was investigated in HepG2 cells. In this study, oxidative stress was induced by arachidonic acid (AA) and iron. Methods : To analyze the hepatoprotective effects of SCGBT against oxidative stress induced by AA + iron, the cell viability, apoptosis-related proteins and intracellular ROS, glutathione (GSH), and mitochondrial membrane permeability (MMP) were measured. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) transcription activation and expressions of Nrf2 target gene were analyzed through immunoblot analysis. Results : SCGBT increased the cell viability from AA + iron - induced cell death and inhibited apoptosis by regulating apoptosis related proteins. SCGBT protected cells by inhibiting ROS production, GSH depletion, and MMP degradation against AA + iron induced oxidative stress. Furthermore, Nrf2 activation was increased by SCGBT, and the Nrf2 target genes were also activated by SCGBT. Conclusions : These results suggest that the SCGBT has a hepatocyte protection effect and antioxidant effect from AA + iron induced oxidative stress.

• The Journal of Korean Medicine
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• v.31 no.6
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• pp.1-7
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• 2010

Objectives: This study was aimed to investigate the effects of Galhwahyejung-tang (GHT) on alcohol-induced oxidative stress in rat model. Methods: Twenty SD rats were orally administrated with 40% ethanol (mL/kg) combined with GHT (50, 100, 200mg/kg) or distilled water for 2 weeks. Biochemistry in blood, malondialdehyde (MDA), total reactive oxygen species (ROS), and total antioxidant capacity (TAC) in serum, liver, brain, and kidney were determined. Results: GHT treatment significantly ameliorated the alcohol-induced alteration of hepatic enzyme; especially AST and ALT. GHT treatment also ameliorated the increase of MDA in liver, ROS level in serum and brain. GHT treatment reduced the depletion of antioxidant capacity in serum and brain. Conclusion: These results that GHT has antioxidant properties explaining the relevance of clinical application and its partial mechanisms of GHT.