Kim, Dong-Jo;Seong, Kum-Soo;Kim, Dong-Won;Kim, Seong-Ruyong;Chang, Che-Chul
Journal of Ginseng Research
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v.28
no.1
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pp.5-10
/
2004
This study was carried out to investigate the effect of the active ingredients from ginseng on paraquat(PQ) toxicity. Oxidative stress was induced by intraperitreatneal injection of PQ at a single dose of 25 mg/kg. Saponin treated groups were given protopanaxadiol saponins(PPD) or protopanaxatriol saponins(PPT)(5 mg/kg, orally) per day for 1, 3, & 7 days. We also investigated the relationship between lipid peroxidation and ginseng saponins by measuring the levels of superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase (GPx), reduced glutathione(GSH), malondialdehyde (MDA), and hydrogen peroxide(H$_2$O$_2$) in liver tissue. The activities of SOD, CAT, and GPx were generally high in the PPD group; the SOD activity on each day was the highest in the PPD group. The H$_2$O$_2$ content was the lowest in the PPD group. The GSH levels were significantly increased in the PPD. The levels of MDA(the end product of lipid peroxidation) were significantly lower in the red ginseng component groups than in the PQ group; the levels were especially low in the PPD groups. These results led us to conclude that the antioxidant effects of extracts from red ginseng prevent oxidative damage by direct antioxidant effects involving SOD, CAT, & GPx, and increasing the ability of the body to synthesize endogenous antioxidants.
Background: Ginsenosides are the main pharmacological components of Panax ginseng root, which are thought to be primarily responsible for the suppressing effect on oxidative stress. Methods: 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and oxygen radical absorption capacity were applied to evaluate the antioxidant activities of the ginsenosides. Human embryonic kidney 293 (HEK-293) cells were incubated with ginsenosides extracted by pulsed electric field (PEF) and solvent cold soak extraction (SCSE) for 24 h and then the injury was induced by $40{\mu}M$$H_2O_2$. The cell viability and surface morphology of HEK-293 cells were studied using MTS assay and scanning electron microscopy, respectively. Dichloro-dihydro-fluorescein diacetate fluorescent probe assay was used to measure the level of intracellular reactive oxygen species. The intracellular antioxidant activities of ginsenosides were evaluated by cellular antioxidant activity assay in HepG2 cells. Results: The PEF extracts displayed the higher 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and stronger oxygen radical absorption capacity (with an oxygen radical absorption capacity value of $14.48{\pm}4.04{\mu}M\;TE\;per\;{\mu}g/mL$). The HEK-293 cell model also suggested that the protective effect of PEF extracts was dose-dependently greater than SCSE extracts. Dichloro-dihydro-fluorescein diacetate assay further proved that PEF extracts are more active (8% higher than SCSE extracts) in reducing intracellular reactive oxygen species accumulation. In addition, scanning electron microscopy images showed that the HEK-293 cells, which were treated with PEF extracts, maintained more intact surface morphology. Cellular antioxidant activity values indicated that ginsenosides extracted by PEF had stronger cellular antioxidant activity than SCSE ginsenosides extracts. Conclusion: The present study demonstrated the antioxidative effect of ginsenosides extracted by PEF in vitro. Furthermore, rather than SCSE, PEF may be more useful as an alternative extraction technique for the extraction of ginsenosides with enhanced antioxidant activity.
Hong, So-hyeon;Hwang, Hwan-Jin;Kim, Joo Won;Kim, Jung A.;Lee, You Bin;Roh, Eun;Choi, Kyung Mook;Baik, Sei Hyun;Yoo, Hye Jin
Journal of Ginseng Research
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v.44
no.4
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pp.664-671
/
2020
Background: Ginsenoside compound-Mc1 (Mc1) is a member of the deglycosylated ginsenosides obtained from ginseng extract. Although several ginsenosides have a cardioprotective effect, this has not been demonstrated in ginsenoside Mc1. Methods: We treated H9c2 cells with hydrogen peroxide (H2O2) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1. The levels of antioxidant molecules, catalase, and superoxide dismutase 2 (SOD2) were measured, and cell viability was determined using the Bcl2-associated X protein (Bax):B-cell lymphoma-extra large ratio, a cytotoxicity assay, and flow cytometry. We generated mice with high-fat diet (HFD)-induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate the antioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1. Results: Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the H9c2 cells. The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1, resulting in a decrease in the production of H2O2-mediated reactive oxygen species. Treatment with ginsenoside Mc1 also significantly reduced the H2O2-mediated elevation of the Bax:Bcl2 ratio and the number of DNA-damaged cells, which was significantly attenuated by treatment with an AMPK inhibitor. Consistent with the in vitro data, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition. Conclusion: Ginsenoside Mc1 decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism, suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases.
The non-vital bleaching technique has been used widely as a very effective treatment method on discolored non-vital teeth. But periodontal tissue deterioration and cervical external root resorption have been reported because of the high toxicity of hydrogen peroxide in bleaching agents. So in previous studies, placement of base over the root canal obturation prior to bleaching has been suggested in order to prevent microleakage of bleaching agents, however, the effectiveness of base is still controversial. The purpose of this study was to evaluate the effects of base and root canal sealer on prevention of leakage of bleaching agents in non-vital bleaching. Fifty-two extracted sound teeth with single root were used. For root canal obturation, Tubuli seal$^{(R)}$(Kerr Co., USA) was used in 39 teeth and in others, AH-26$^{(R)}$(De Trey Dentsply, Inc., Switzerland) was used as a root canal sealer. 26 teeth among the teeth obturated with Tubuli seal$^{(R)}$ were divided into two groups, and Dentin cement$^{(R)}$(GC corp., Japan) and JRM$^{(R)}$(De Trey Dentsply, Inc. Germany) were used in each group as a intracanal base. In all teeth, non-vital bleaching using bleaching agent mixed with methylene blue dye was performed and all specimens were stored in $37^{\circ}C$ water bath for 72 hours. After sectioning longitudinally, the depth of dye leakage was measured with digital vernier calipers under the stereobinocular microscope using ${\times}40$ magnification. It can be concluded as follows: 1. The microleakage of bleaching agent was observed ill all groups regardless of type of the base and the sealer. 2. The microleakage in the groups using AH-26$^{(R)}$ as a sealer was significantly reduced (p<0.05). 3. In the groups with intracanal base, micro leakage was observed through almost the whole depth of the base and there was no significant difference between Dentin cement$^{(R)}$ and IRM$^{(R)}$ group(p>0.05). In conclusion, all the basing materials and the sealers in this study did not prevent the microleakage of bleaching agent. Therefore further studies and attempts to seal off the pulp chamber will be necessary.
The photocatalytic degradation of trichloroethlylene (TCE), has been investigated over $TiO_2$ photocatalysts irradiated with solar light. The effect of operational parameters, i.e., initial TCE concentration, $TiO_2$ concentration, pH and additives ($H_2O_2$, persulphate($S_2O{_8}^-$)) on the degradation rate of aqueous solution of TCE has been examined. The results presented in this work demonstrated that degradation of the TCE with $TiO_2/solar$ light was enhanced by augumentation in $TiO_2$ loading, pH, and adding additives but was inhibited by increase in initial TCE concentration. Also individual use of $H_2O_2$ was far more effective than using persulphate in TCE removal efficiency. Furthermore, the relative toxicity with a $solar/TiO_2/H_2O_2$ system was about 15% lower than with a $solar/TiO_2/persulphate$ system and about 35% lower than with a $solar/TiO_2$ system within a reaction time of 150 min, respectively.
In this experiment, photochemical reaction has been applied to destroy TCE in water phase. The main target of this work is to investigate the technical feasibility of large scale of solar detoxification reactor for water treatment. The results have revealed that solar detoxification utilizing photon energy from the sun is the most attractive process to decompose organic toxins in water phase at room temperature. The detailed results from this work are as follows; (1) The highest conversion ratio of TCE was obtained by using $TiO_2$, annatase as a photocatalyst among $TiO_2$ anatase, $TiO_2$ rutile and $V_2O_5$ under the same experimental condition. The anatase crystal structure was confirmed with XRD analysis, and its surface area was 7.748 $m^2/g$ from the BET-$N_2$ measurement (2) 0.1 wt% of $TiO_2$ anatase has been adopted as optimal quantity for batch slurry reactor at this experimental conditions. (3) The effect of hydrogen peroxide on the conversion of TCE was investigated. Its optimal quantity was 0.06 vol. % under this experimental conditions. (4) The effect of oxygen on the conversion of TCE also was studied by controlling the head space in photoreactor. Results indicated that sufficient amount of oxygen should be supplied to accomplish the highest conversion rate of TCE in water phase.
For the induction of arthropathy, 4% hydrogen peroxide ($H_2O_2$) was injected for 4 weeks into the intra-articular space of the 25 New Zealand white rabbits to damage articular cartilage. The verification of arthropathy induction and the effect of scan-bio laser treatment were determined by measuring superoxide dismutase (SOD) activity, by observing gross and histopathologic findings. The SOD activity increased by about 40% in arthropathy group, as compared to controls. Although SOD activity in arthropathy group was not significantly different from the 2-week group, it was significantly different from the 4-week control and treatment groups. There was also a significant difference between the 4-week control and treatment groups. Grossly, erosions formed on the articular cartilage surface, and the lateral femoral condyle was damaged in arthropathy group. In comparison, there was slight, but not significant, progression of the lesion in the 2-week control group, and no difference between the 2-week treatment and control groups. Conversely, severe erosions damaged the articular cartilage in the 4-week control group. Cartilage proliferation was seen in gross observations in the 4-week treatment group, suggesting a treatment effect. Histopathologically, there was slight articular surface damage and apoptosis in arthropathy group, and serious cartilage damage, despite slight chondrocyte proliferation, in the 4-week control group. By contrast, the 4-week treatment group showed chondrocyte replacement, with close to normal articular cartilage on the articular surface. There was significant cartilage proliferation with regeneration of the articular cartilage on the articular surface in the group treated with low-level laser, as compared to control group, when arthropathy was induced by $H_2O_2$ injections. Therefore, low-level laser was effective in the treatment of chemically induced arthropathy.
Paraquat, the representative bipyridilium herbicide, has high phytotoxic activity through generating toxic oxygen species such as superoxide, hydrogen peroxide and hydroxy radical. The response patterns of plants to paraquat were various. It was assumed that the different response was derived from different antioxidative mechanisms including antioxidative enzymes and antioxidant. Paraquat treatment increased reducing sugar content and malondialdehyde formation at 35 days after treatment in a dose-dependent manner but chlorophyll content decreased. Glutathione content increased by paraquat treatment and tolerant species showed more glutathione content than susceptible species. Superoxide dismutase activity increased with the increase in paraquat concentration and that was higher in tolerant species than susceptible species. Photosynthetic activity(PSII activity) was affected by paraquat, so the susceptible species showed more reduced oxygen evolving capacity than tolerant species. Catalse, NADPH-cytochrome C reductase, and malate dehydrogenase, the enzymes tested in this study, showed that the activities decreased by paraquat treatment. Further studies are necessary to determine whether antioxidative system cause the tolerance to paraquat.
Park, Sang-Won;Kim, Cheol-Hong;Youn, Hyoun-Min;Jang, Kyung-Jeon;Ahn, Chang-Beohm;Song, Choon-Ho
Korean Journal of Acupuncture
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v.24
no.1
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pp.171-187
/
2007
Objectives : This study was performed to determine if Orostachys japonicus A. Berger herbal acupuncture (OjB) provides the protective effect against the loss of cell viability and DNA damage induced by oxidant in renal proximal tubular cells. Methods : The cell viability was evaluated by a MTT reduction assay and DNA damage was estimated by measuring double stranded DNA breaks in opossum kidney (OK) cells, an established proximal tubular cell line. Lipid peroxidation was determined by measuring malondialdehyde (MDA), a product of lipid peroxidation. Results : H2O2 increased the loss of cell viability in a time-dependent manner, which were prevented by 0.1% OjB. The protective effect of OjB was dose-dependent over concentration range of 0.05-0.5%. H2O2 caused ATP depletion and DNA damage, which were prevented by OjB and the hydrogen peroxide scavenger catalase. The loss of cell viability by H2O2 was not affected by the antioxidant DPPD, but lipid peroxidation by the oxidant was completely inhibited by DPPD. Generation of superoxide and H2O2 in neutrophils activated by phorbol-12,13-dibutyrate was inhibited by OjB in a dose-dependent manner. OjB inhibited generation of H2O2 in OK cells treated with antimycin A and exerted a direct H2O2 scavenging effect. Exposure of OK cells to 1 mM tBHP caused a significant depletion of glutathione which was prevented by OjB. OjB accelerated the recovery in cells cultured for 20 hr in normal medium without oxidant following oxidative stress. Conclusions : These results suggest that OjB exerts the protective effect against oxidant-induced cell injury and its protective effect was resulted from radical scavenging and antioxidant activities.
Graphene is an allotrope of carbon that is composed of one-atom-thick planar sheets. It is known to have a preventive effect on cancer in photothermal therapy and a protective effect in DNA oxidation. The effect of graphene on oxidative stress and matrix metalloproteinases (MMPs) was investigated in human fibrosarcoma HT1080 cells. The results showed that graphene specifically exerted an inhibitory effect on DNA oxidation, but it did not inhibit other oxidative stress. In addition, graphene decreased the expression and the activation of MMP-2 and MMP-9 stimulated by phenazine methosulfate-m, which induces the production of intracellular hydrogen peroxide. In particular, the expression of antioxidant enzymes, such as superoxide dismutase (SOD-2), was decreased in the HT1080 cells, indicating that the decrease in the expression level of SOD was due to the antioxidant effect of graphene. These results suggest that the inhibitory effect of oxidative stress in the presence of graphene could inhibit the expression of MMPs in HT1080 cells. Based on the above results, graphene may have chemoprevention properties through inhibition of MMP-2 and MMP-9 related to metastasis.
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