• Nutrition Research and Practice
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• v.8 no.2
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• pp.138-145
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• 2014

BACKGROUND/OBJECTIVES: This study was performed to investigate the in vitro antioxidant and cytoprotective effects of fermented sesame sauce (FSeS) against hydrogen peroxide ($H_2O_2$)-induced oxidative damage in renal proximal tubule LLC-PK1 cells. MATERIALS/METHODS: 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl radical ($^{\bullet}OH$), and $H_2O_2$ scavenging assay was used to evaluate the in vitro antioxidant activity of FSeS. To investigate the cytoprotective effect of FSeS against $H_2O_2$-induced oxidative damage in LLC-PK1 cells, the cellular levels of reactive oxygen species (ROS), lipid peroxidation, and endogenous antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) were measured. RESULTS: The ability of FSeS to scavenge DPPH, $^{\bullet}OH$ and $H_2O_2$ was greater than that of FSS and AHSS. FSeS also significantly inhibited $H_2O_2$-induced ($500{\mu}M$) oxidative damage in the LLC-PK1 cells compared to FSS and AHSS (P < 0.05). Following treatment with $100{\mu}g/mL$ of FSeS and FSS to prevent $H_2O_2$-induced oxidation, cell viability increased from 56.7% (control) to 83.7% and 75.6%, respectively. However, AHSS was not able to reduce $H_2O_2$-induced cell damage (viability of the AHSS-treated cells was 54.6%). FSeS more effectively suppressed $H_2O_2$-induced ROS generation and lipid peroxidation compared to FSS and AHSS (P < 0.05). Compared to the other sauces, FSeS also significantly increased cellular CAT, SOD, and GSH-px activities and mRNA expression (P < 0.05). CONCULUSIONS: These results from the present study suggest that FSeS is an effective radical scavenger and protects against $H_2O_2$-induced oxidative damage in LLC-PK1 cells by reducing ROS levels, inhibiting lipid peroxidation, and stimulating antioxidant enzyme activity.

• Journal of Periodontal and Implant Science
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• v.25 no.3
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• pp.497-517
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• 1995

The cells associated with normal defense mechanism in inflammation release free oxygen radicals, hydroxy radicals, and various protease, all of which can damage the surrounding cells(fibroblasts) and matrix molecules(collagen). The objective of this study was to evaluate the effects of "scavenger" enzyme, superoxide dismutase(SOD). to periodontal ligament (PDL) cells. Human PDL cells were cultured from the teeth extracted for non-periodontal reason. Cultured PDL cells in vitro were treated with SOD and LPS according to dosage and culture times. Cellular activity was exaimed by Microtitration(MTT) assay. The quantitative expression of cellular proliferation by proliferating cell nuclear antigen(PCNA), collagen type I and fibronectin by indirect immunocytochemically stain in PDL cells were done. The results were as follows: 1. As only SOD treated group at 2 and 3 days, PDL cell activity was significantly increased at more than 150U(P<0.05). 2. When LPS(0.5, $5{\mu}g/m{\ell}$) and SOD(more than 150U) were added together, it was significantly increased than LPS only treated and control groups at 2 days(P<0.05). 3. When LPS($5{\mu}g/m{\ell}$) and SOD(150, 300U) were added together, PCNA index was significantly increased than LPS only treated and control groups at 2 and 3 days(P<0.05). 4. When LPS($5{\mu}g/m{\ell}$) and SOD(150U) were added together, collagen type I was significantly increased than LPS only treated and control groups at 3 days(P<0.05). 5.When LPS($5{\mu}g/m{\ell}$) and SOD(300U) were added together, fibronectin was significantly increased than LPS only treated and control groups at 3 days(P<0.05). On the above the results, the SOD in association with collagen type I, fibonectin, and PCNA may afford biological protection to oxy-radicals that were typically liberated during normal inflammatory response. Thus, the exogenous application of SOD may be effective in sthe treatment of the localized breakdown associated with chronic periodontal disease.

• The Journal of Internal Korean Medicine
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• v.21 no.1
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• pp.13-22
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• 2000

목적 : 본(本) 연구(硏究)는 배기음(排氣飮)이 인간(人間)의 장관내(腸管內)에서 산화물(酸化物)에 의해 유발(誘發)된 세포(細胞)의 사망(死亡) 및 DNA의 손상(損傷)을 방지할수 있는지를 검증(檢證)하기 위한 실험(實驗)이다. 방법 : 배양(培養)된 인체장관(人體腸管) 세포계열(細胞系列)인 Caco-2 세포(細胞)에서 세포(細胞)의 사망(死亡)은 trypan bile의 소실정도에 의해서 평가했으며, DNA의 손상(損傷)은 double stranded DNA의 파괴정도를 측정하여 평가하였다. $H_2O_2$는 표본(標本) 산화제(酸化劑)로 사용되었다. 결과 : $H_2O_2$에 노출된 세포들의 세포사망(細胞死亡) 정도는 노출시간과 용량에 비례하여 증가하는 양상을 보였다. 배기음(排氣飮)은 $H_2O_2$에 의해 유발(誘發)되는 세포방지를 방지하였고, 0.05-1%의 농도범위에 걸쳐서는 그 효과가 용량에 비례하여 증가하는 양상을 보였다. $H_2O_2$에 의해 유발(誘發)된 세포손상(細胞損傷)은 catalase(hydrogen peroxide scavenger enzyme)와 deferoxamine(iron chelator)에 의해 억제되었다. 그러나 강력한 항산화제(抗酸化劑)인 DPPD는 $H_2O_2$에 의해 유발(誘發)되는 세포손상(細胞損傷)에는 영향을 주지 못했다. $H_2O_2$에 의해 유발(誘發)된 지질(脂質)의 과산화(過酸化)는 배기음(排氣飮)과 DPPD에 의해 억제되었다. $H_2O_2$에 의해 유발(誘發)된 DNA의 손상(損傷)은 배기음(排氣飮)에 의해 방지되었으며 용량에 의존하는 양상을 보였다. $H_2O_2$에 의해 유발(誘發)된 DNA의 손상은 catalase와 deferoxamine에 의해 억제되었지만 DPPD는 억제시키지 못했다. 배기음(排氣飮)은 $H_2O_2$에 의해 유발(誘發)된 ATP의 소실을 회복시켰다. 이러한 실험결과 $H_2O_2$에 의해 유발(誘發)된 세포(細胞)의 손상(損傷)은 지질(脂質)의 과산화(過酸化)와는 다른 독립적인 기전에 의해 일어남을 나타낸다. 결론 : 이러한 결과들로 볼 때 Caco-2 세포(細胞)에서 배기음(排氣飮)이 항산화작용(亢酸化作用)보다는 다른 기전을 통하여 Caco-2 세포안에서 산화제(酸化劑)에 의해 유발(誘發)된 세포(細胞)의 사망(死亡)와 DNA의 손상(損傷)을 방지할 수 있다는 것을 가리킨다. 따라서 본 연구(硏究)는 배기음(排氣飮)이 반응성산소기(反應性酸素基)에 의해 매개된 인체(人體) 위장관질환(胃腸管疾患)의 치료(治療)에 사용할 수 있을 가능성(可能性)이 있음을 제시하고 있다.

• Preventive Nutrition and Food Science
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• v.5 no.4
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• pp.213-218
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• 2000

The purpose of the study was to investigate the effects of dietary green tea catechin and vitamin E on the phospholipse {TEX}$A_{2}${/TEX} activity and th antioxidative defense system in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley male rats weighing 100$\pm$10 gm were randomly assigned to one normal and five STZ-induced diabetic groups. The diabetic groups were assigned either a catechin-free diet (DM group), 0.5% catechin diet (DM-0.5C group), 1% catechin diet (DM-1C group), vitamin E-free diet (DM-0E group), and 400 mg vitamin E per kg diet (DM-400E group) according to the levels of dietary catechin or vitamin E supplementation. The vitamin E levels of the normal, DM, DM-0.5C, and DM-1C groups were 40 mg per kg diet. Diabetes was experimentally induced by an intravenous injection of streptozotocin after 4 weeks of feeding the five experimental diets. The animals were sacrificed on the 6th day of he diabetic state. The body weight gains were lower in all five diabetic groups after the STZ injection. The platelet phospholipase {TEX}$A_{2}${/TEX}({TEX}$PLA_{2}${/TEX}) activity in the diabetic groups was higher than that in the normal group. However, the enzyme activity in the DM-0.5C, DM-1C, and DM-400E groups was lower than that in the DM and DM-0E groups. The cytochrome {TEX}$P_{450}${/TEX} and cytochrome {TEX}$b_{5}${/TEX} content and NADPH-cytochrome {TEX}$P_{450}${/TEX} reductase activity were about 50~110% higher in the DM and DM-0E groups than in the normal group, yet significantly reduced by either catechin or vitamin E supplementation. The superoxide dismutase (SOD) content in the liver did not differ significantly in any of the groups. However, the glutathione peroxidase (GSHpx) activity was generally lower in the diabetic groups, compared with the normal group, whereas that of the DM-0.5C, DM-1C, and DM-400E groups was significantly higher compared with that of the DM and DM-0E groups. The levels of thiobarbituric acid reactive substances (TBARS) in the liver tissue were 148% and 201% higher in the DM and DM-0E groups, respectively, compared with the normal group, however, these levels were reduced by either catechin or vitamin E supplementation (DM-0.5, DM-1C and DM-400E). Accordingly, the present results indicate that STZ-induced diabetic rats exhibited an imbalance between free radical generation and scavenger systems in the liver which led to the acceleration of lipid peroxidation. However, these abnormalities were reduced and the antioxidative defense system was restored by either dietary catechin or vitamin E supplementation. In conclusion, the effects of dietary catechin or vitamin E in streptozotocin-induced diabetic rats would appear to inhibit lipid peroxidation as an anti-oxidant by regulating the activity of {TEX}$PLA_{2}${/TEX}.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.1
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• pp.110-117
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• 1996

To evaluate the feeding effect of oriental medicine on the functional properties of pork, male pigs(Sus scrofa var. domesticus L.) were fed commercial basic diets containing 1.0%, 3.0% and 7.0% of oriental medicine complex from 30 or 45 days before slaughter. The growth pattern and physical conditions of pigs during the feeding period were checked, and after slaughter, the taste of pork and biological characteristics of serum were analyzed. Body weight gain was significantly increased in case of 45 day feeding groups of 3.0 and 7.0% compared with control group (p<0.05), whereas food intakes were slightly decreased in these groups. Triglyceride and total cholesterol levels were effectively decreased in the same feeding groups compared with control group (p<0.01~0.001). Three percent feeding group not only effectively decreased the LDL-cholesterol levels, but also sig-nificantly decreased the atherogenic index in 30 days(p<0.001). Malondialdehyde levels and hy-droxyl radical formations were effectively inhibited in all oriental medicine feeding groups. Superoxide dismutase activities were effectively increased only in 3.0% feeding groups, HDL-cholesterol levels almost did not change in 3.0% and 7.0% feeding groups in 30 days. External and sensory evaluations make satisfactory results in all oriectal medicines feeding groups. According to the experimental results, the growth pattern and physical nomditions of the pigs fed oriental medicine without feeding any antibiotics were relatively superior to those of control group. The authors suggest that, if more than 3.0% of oriental medicine were fed to the pigs from more then 30 days before slaughter the pork is reatively better than those of general pork not only for the modulating the chronic degenerative diseases, but also for its qualities and tastes.

• BMB Reports
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• v.48 no.7
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• pp.395-400
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• 2015

Parkinson's disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP⁺) induced SH-SY5Y neuronal cell death and in a 1-methyl-4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP⁺-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases. [BMB Reports 2015; 48(7): 395-400]

• Journal of Life Science
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• v.26 no.1
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• pp.8-16
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• 2016

Reactive oxygen species (ROS), at appropriate concentrations, mediate various normal cellular functions, including defense against pathogens, signal transduction, cellular growth, and gene expression. A recent study demonstrated that ROS and ROS-generating NADPH oxidase (Nox) are important in self-renewal and neuronal differentiation of subventricular zone (SVZ) neural stem cells in adult mouse brains. In this study, we found that endogenous ROS were detected in SVZ neural stem cells cultured from postnatal mouse brains. Nox4 was predominantly expressed in cultured cells, while the levels of the Nox1 and Nox2 transcripts were very low. In addition, the Nox4 gene was highly upregulated (by up to 10-fold) during neuronal differentiation. Immunocytochemical analysis detected the Nox4 protein mainly in neurons positive for the neuronal specific tubulin Tuj1. After differentiation, endogenous ROS were detected exclusively in neuron-like cells with processes. In addition, perturbation of the cellular redox state with N-acetyl cysteine, a ROS scavenger, during neuronal differentiation greatly inhibited neurogenesis. Lastly, knockdown of Nox4 using short hairpin RNA decreased neurogenesis. These findings suggest that Nox4 may be a major ROS-generating enzyme in postnatal SVZ neural stem cells, and Nox4-mediated ROS generation may be important in their neuronal differentiation.

• Journal of Life Science
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• v.18 no.3
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• pp.323-328
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• 2008

In this study we evaluated the method to develop red ginseng oil containing high content of phytochemicals by enzymes treatment. To select the optimum extraction process of red ginseng with oils, the antioxidant activities of red ginseng using various enzymes were measured. Red ginseng after 0.5% cellulase treatment for 1 hr at $50^{\circ}C$ had higher antioxidant activity than the other conditions. We found that red ginseng/soybean oil extracted for 15 days at $40^{\circ}C$ after 0.5% cellulase treatment increased DPPH radical scavenger activity and decreased the TBA and POV values. However, red ginseng/olive oil had little functional activities compare to the red ginseng/soybean 0il. We also analyzed vitamin A and E by HPLC and found that vitamin E was increased by 0.5% cellulase treatment in the oil. This is the first report that red ginseng oil extracted by enzyme treatment has various beneficial effects.

• Journal of Life Science
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• v.26 no.9
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• pp.1022-1026
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• 2016

In this study the hot water extract was prepared from Hydrocotyle sibthorpioides (Araliaceae) leaves and stems to study antioxidant activities and lipoxygenase inhibition. The extract showed the protective hydroxyl radical (-OH) which can damage virtually all types of macromolecules: carbohydrates, nucleic acids (mutations), lipids (lipid peroxidation), and amino acids. Hydroxyl radical scavenging activity of H. sibthorpioides was 78.6%. The extract showed strong activity against 1, 1- diphenyl 2-picrylhyorazyl (DPPH) which is a well-known radical and a trap (scavenger) for other radicals. DPPH scavenging activity of leaves of H. sibthorpioides was evaluated at 8.0 mg/ml was 86.0%. Lipoxygenases (LOXs) constitute a heterogeneous family of lipid peroxidizing enzymes capable of oxygenating polyunsaturated fatty acids to their corresponding hydroperoxy derivatives. The inhibitory effect of 15-LOX by H. sibthorpioides was assayed using a Morgan microplate assay. The extract of H. sibthorpioides was 55.5% inhibitory effects on the inhibition of LOX at 8.0 mg/ml. The IC₅₀ values for OH activity, DPPH activity, and LOX inhibition from leaves 5.23 mg/ml, 6.44 mg/ml, and 3.71 mg/ml, respectively. Antioxidative activity assay showed that the water extracts from leaf and stem had a strong reducing power. These results show that H. sibthorpioides has some phytochemical constituents which may be active against the free radicals (OH and DPPH) and lipoxygenase enzyme.

• Korean Journal of Food Science and Technology
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• v.41 no.1
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• pp.93-99
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• 2009

This study aimed to determine whether or not glycoprotein isolated from Cudrania tricuspidata Bureau fruit(CTB glycoprotein) exerts a hepatoprotective effect on liver injury induced by the administration of carbon tetrachloride($CCl_4$, 1.0mL/kg) to A/J mice. Following the administration of CTB glycoprotein(0-20mg/kg), the activities of antioxidant enzymes (superoxide dismutase(SOD), catalase(CAT), and glutathione peroxidase(GPx)), and the quantities of measured thiobarbituric acid reactive substances(TBARS), lactate dehydrogenase(LDH), and nitric oxide(NO) were evaluated from the murine liver tissues and plasma. Additionally, the activity of nuclear factor-kappa B(NF-${\kappa}B$) was assessed after pretreatment with $CCl_4$. When the mice were treated with $CCl_4$ alone, the activities of antioxidative enzymes reduced but amounts of TBARS, LDH, and NO increased. However, the results of treatment with CTB glycoprotein(10 and 20 mg/kg) revealed significantly increased activities of antioxidant enzymes(SOD, CAT, and GPx), as compared with $CCl_4$ alone. On the other hand, the result showed significant diminutions of the quantities of TBARS, LDH, and NO after treatment with CTB glycoprotein(10 and 20 mg/kg), as compared to $CCl_4$ alone. The activity of NF-${\kappa}B$ also declined after pretreatment with CTB glycoprotein, as compared with $CCl_4$ treatment alone. Thus, it is suggested that the CTB glycoprotein exerts a protective effect against $CCl_4$-induced liver injury in A/J mice.