• 제목/요약/키워드: sod gene

검색결과 226건 처리시간 0.025초

정전가매이진탕(正傳加味二陳湯)이 과산화지질 급여 비만 쥐의 지질강하, 항산화효과 및 염증매개물질의 생산에 미치는 영향 (Effects of Jengjengamiyijin-tang (zhengzhuanjiaweierchentang) on Lowering Lipid, Antioxidation and Production of Inflammatory Mediators Being Used Rats Fed on High Oxidized Fat)

  • 허성규;박원형;차윤엽
    • 한방재활의학과학회지
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    • 제23권4호
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    • pp.9-21
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    • 2013
  • Objectives The purpose of this study was investigating effects of Jengjengamiyijin-tang (zhengzhuanjiaweierchentang) (JGYT) on lowering lipid, antioxidation and production of inflammatory mediators being used rats fed on high oxidized fat. Methods We divided fat Sprague-Dawley rats fed on high oxidized into 4 groups. Each of 8 rats was divided into a control group and experimental groups. We fed a control group of rats a basal diet and administered normal saline (100 mg/kg, 1 time/1 day) for 4 weeks. And We fed each experimental group of rats basal diet and administered an extract of JGYT extracts (100 mg/kg, 200 mg/kg, 300 mg/kg, 1 time/1 day) for 4 weeks. At the end of the experiment, the rats were sacrificed to determine their chemical composition. We measured lipid of plasma and liver, concentration of proinflammatory cytokines, antioxidative activity and plasma tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), plasma interleukin-6 (IL-6), Apo-B, Apo-E and Leptin gene expression. Results 1. Concentration of plasma FFA, LDL-cholesterol, plasma and liver total cholesterol showed a significant decrement in JGYT groups. However, concentration of plasma HDL-cholesterol showed a significant increment in JGYT groups. 2. Concentration of plasma and liver TG, TBARS showed a significant decrement in JGYT groups. However, concentration of liver GSH-Px, SOD and CAT showed a significant increment in JGYT groups. 3. Plasma GPT activity and concentration of plasma IL-6, TNF-${\alpha}$, NO, Ceruloplasmin, ${\alpha}1$-acid glycoprotein showed a significant decrement in JGYT groups. 4. In the analysis of RT-PCR, gene expression of Apo-B and Apo-E in the JGYT groups showed a low expression than that of control group. However, the gene expression of leptin showed no difference in all the treatment groups. 5. The ratio of leptin expression per ${\beta}$-actin expression showed no significant difference among all treatment groups. However, The ratio of Apo-B and Apo-E expression per ${\beta}$-actin expression showed a significant decrement in JGYT groups. Conclusions According to this study, extract of JGYT showed a positive effect in lowering lipid, antioxidation and control of inflammatory mediators production.

홍국(Monascus purpureus)쌀을 첨가한 고콜레스테롤 식이가 흰쥐의 항산화 활성에 미치는 영향 (Effect of Red Yeast (Monascus purpureus) Rice Supplemented Diet on Lipid Profiles and Antioxidant Activity in Hypercholesterolemic Rats)

  • 권정숙
    • 한국식품영양과학회지
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    • 제43권1호
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    • pp.16-23
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    • 2014
  • 고콜레스테롤 식이에 홍국쌀 분말을 0.2%, 1% 및 5% 첨가한 식이를 4주간 섭취한 동물에서 홍국쌀의 지질 개선 효과와 함께 항산화 효과를 혈액과 간의 항산화 효소 활성, 항산화 효소의 유전자 발현 및 DNA 손상에 미치는 영향으로 분석하였다. 홍국쌀 분말 첨가 식이를 섭취한 후의 체중 변화, 식이섭취량, 식이 효율 및 간 무게는 대조군과 유의한 차이가 없었다. 혈장에서 총 콜레스테롤은 대조군에 비해 0.2% 첨가군에서 24% 감소하였으며, HDL 콜레스테롤은 5% 첨가군에서 20% 증가하였고 LDL 콜레스테롤은 0.2% 첨가군에서 42% 감소한 것으로 나타났다. 항산화 효소 활성에서는 SOD 활성이 감소하거나 유의성이 없었으나 적혈구에서 GPx와 CAT의 활성이 대조군에 비해 유의성 있게 증가하는 것으로 나타났으며, 간의 TBARS는 5% 첨가군에서 대조군에 비해 19% 유의적으로 감소한 것으로 나타났다. 항산화 효소의 유전자 발현에서는 5% 첨가군에서 CAT의 발현이 대조군에 비해 7.9배 유의성 있게 증가하였다. 홍국쌀 분말 섭취로 인한 DNA 손상은 관찰되지 않았으며, $H_2O_2$로 산화 스트레스를 가했을 때 DNA 손상이 농도 의존적으로 억제되는 것으로 나타났다. 이상의 결과로부터 홍국쌀의 섭취가 혈액과 간의 지질 대사 개선 효능을 가지며, 항산화효소의 활성화를 통해 ROS에 의한 세포 손상을 억제할 뿐 아니라 LDL 콜레스테롤의 산화도 억제할 것으로 예상되므로 심혈관계 질환에 대한 예방 효과가 있을 것으로 사료된다.

산화적 스트레스에 대한 고온고압처리 인삼의 억제 효과 (Inhibitory Effects of Panax ginseng C. A. Mayer Treated with High Temperature and High Pressure on Oxidative Stress)

  • 윤보라;이영준;홍희도;이영철;김영찬;이영경;김경탁;이옥환
    • 한국식품영양학회지
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    • 제25권4호
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    • pp.800-806
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    • 2012
  • 체내에서 산화스트레스에 의해 생성되는 활성산소종(reacitve oxygen species, ROS)은 당뇨병, 비만 등과 같은 만성질환을 야기시키는 것으로 알려져 있다. 고려인삼(Panax ginseng)은 수천 년간 피로 회복 및 면역증강용 기능성식품으로 이용되어 왔고, 사포닌, 산성다당체, 페놀성 화합물과 같은 다양한 생리활성 물질을 함유하고 있다. 따라서 본 연구에는 고온, 고압처리하여 제조한 신규 인삼에 대한 산화적 스트레스 저감 효능을 평가하고자 하였다. C2C12 근육세포에 산화적 스트레스를 유도하기 위해 $H_2O_2$ 1 mM 처리하고, 전처리 조건을 달리한 인삼 시료를 처리하여 cell morphology 및 항산화 관련 유전자인 SOD, CAT 및 GPx를 살펴보았고, 3T3-L1 지방세포는 분화과정 중 ROS 생성 억제효과 및 CAT, GPx 및 Cu/Zn-SOD의 항산화효소 관련 유전자의 발현 정도를 조사하였다. 고온, 고압처리한 인삼은 산화적 스트레스가 유도된 C2C12 근육세포 및 3T3-L1 지방세포에서 유의적으로 산화적 스트레스를 저감하는 것으로 나타났다. 이상의 결과로 보아, 본 연구진에 의해 개발된 고온 및 고압 처리된 인삼은 항산화 및 항피로 효능이 기대되는 바이며, 본 연구는 동물세포 수준에서의 비교이며, 보다 정확한 작용기전의 구명을 위해 향후 추가적인 연구를 통한 비교 실험이 수행되어야 할 것으로 사료된다.

Schizosaccharomyces pombe에 존재하는 bacterioferritin comigratory protein의 고온 스트레스에 대한 열저항적 성질 (Thermoresistant properties of bacterioferritin comigratory protein against high temperature stress in Schizosaccharomyces pombe)

  • 류인왕;이수희;임혜원;안기섭;박광학;사재훈;정경진;임창진;김경훈
    • 미생물학회지
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    • 제52권4호
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    • pp.398-405
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    • 2016
  • 이전의 연구에서, bacterioferritin comigratory protein (BCP)을 인코딩하는 Schizosaccharomyces pombe의 구조유전자를 shuttle vector인 pRS316에 클로닝하여 BCP 과잉발현 플라즈미드인 pBCP10을 제조한 바 있다. 본 연구에서는, 플라즈미드 pBCP10을 사용하여 고온 스트레스에 대한 BCP의 열저항적 성질을 평가하였다. 대수기의 초기까지 성장시킨 S. pombe 세포의 배양 온도를 $30^{\circ}C$에서 $37^{\circ}C$$42^{\circ}C$로 전이시키는 경우, pBCP10 함유 S. pombe 세포가 벡터 대조 세포보다 $37^{\circ}C$$42^{\circ}C$ 모두에서 유의하기 더 잘 성장하였다. 높은 배양 온도로 전이한 뒤 6시간에서, pBCP10 함유 S. pombe 세포가 벡터 대조 세포보다 낮은 활성산소종(ROS)과 일산화질소(NO)의 지표로 측정된 아질산염(nitrite) 함량을 갖고 있음이 확인되었다. 온도 전이 뒤에, 총 글루타치온(total glutathione) 함량과 총 수퍼옥사이드 디스뮤타제(superoxide dismutase) 활성은 대응되는 벡터 대조 세포보다 pBCP10 함유 S. pombe 세포에서 현저하게 높다는 사실도 확인되었다. 종합하면, S. pombe BCP는 열저항적 역할을 보유하는 데, 활성산소종과 일산화질소에 대한 하강시키는 활성과 총 글루타치온과 수퍼옥사이드 디스뮤타제 등의 항산화 성분들을 상승시키는 활성, 즉 종합적으로 열안정성을 유지하는 활성에 근거하는 것으로 추정되었다

Melatonin Attenuates Nitric Oxide Induced Oxidative Stress on Viability and Gene Expression in Bovine Oviduct Epithelial Cells, and Subsequently Increases Development of Bovine IVM/IVF Embryos

  • Kim, J.T.;Jang, H.Y.;Park, C.K.;Cheong, H.T.;Park, I.C.;Yang, B.K.
    • Asian-Australasian Journal of Animal Sciences
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    • 제24권2호
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    • pp.190-197
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    • 2011
  • The objective of the present study was to elucidate the fundamental mechanism of bovine oviduct epithelial cell (BOEC) co-culture on developmental capacity of bovine IVM/IVF embryos and to determine whether or not melatonin acts as an antioxidant in BOEC culture and subsequent embryo development. These studies examined the effects of melatonin against NO-induced oxidative stress on cell viability, lipid peroxidation (LPO) and the expression of antioxidant genes (CuZnSOD, MnSOD and Catalase) or apoptosis genes (Bcl-2, Caspase-3 and Bax) during BOECs culture. We also evaluated the developmental rates of bovine IVM/IVF embryos with BOEC co-culture, which were pre-treated with melatonin ($1,000\;{\mu}M$) in the presence or absence of sodium nitroprusside (SNP, $1,000\;{\mu}M$) for 24 h. Cell viability in BOECs treated with SNP (50-$2,000\;{\mu}M$) decreased while melatonin addition (1-$1,000\;{\mu}M$) increased viability in a dose-dependent manner. Cell viability in melatonin plus SNP ($1,000\;{\mu}M$) gradually recovered according to increasing melatonin addition (1-$1,000\;{\mu}M$). The LPO products were measured by thiobarbituric acid (TBA) reaction for malondialdehyde (MDA). Addition of melatonin in BOEC culture indicated a dose-dependent decrease of MDA, and in the SNP group among BOECs treated with SNP or melatonin plus SNP groups MDA was significantly increased compared with SNP plus melatonin groups (p<0.05). In expression of apoptosis or antioxidant genes detected by RT-PCR, Bcl-2 and antioxidant genes were detected in melatonin or melatonin plus SNP groups, while Caspase-3 and Bax genes were only found in the SNP group. When bovine IVM/IVF embryos were cultured for 6-7 days under the BOEC co-culture system pre-treated with melatonin in the presence or absence of SNP, the highest developmental ability to blastocysts was obtained in the $1,000\;{\mu}M$ melatonin group. These results suggest that melatonin has an anti-oxidative effect against NO-induced oxidative stress on cell viability of BOECs and on the developmental competence of bovine IVM/IVF embryo co-culture with BOEC.

엽록체 항산화기구 대사조절에 의한 환경스트레스 내성 식물 (Transgenic Plants with Enhanced Tolerance to Environmental Stress by Metabolic Engineering of Antioxidative Mechanism in Chloroplasts)

  • 권석윤;이영표;임순;이행순;곽상수
    • Journal of Plant Biotechnology
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    • 제32권3호
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    • pp.151-159
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    • 2005
  • Injury caused by reactive oxygen species (ROS), known as oxidative stress, is one of the major damaging factors in plants exposed to environmental stress. Chloroplasts are specially sensitive to damage by ROS because electrons that escape from the photosynthetic electron transfer system are able to react with relatively high concentration of $O_2$ in chloroplasts. To cope with oxidative stress, plants have evolved an efficient ROS-scavenging enzymes such as superoxide dismutase (SOD) and ascorbate peroxidase (APX), and low molecular weight antioxidants including ascorbate, glutathione and phenolic compounds. To maintain the productivity of plants under the stress condition, it is possible to fortify the antioxidative mechanisms in the chloroplasts by manipulating the antioxidation genes. A powerful gene expression system with an appropriate promoter is key requisite for excellent stress-tolerant plants. We developed a strong oxidative stress-inducible peroxidase (SWPA2) promoter from cultured cells of sweetpotato (Ipomoea batatas) as an industrial platform technology to develop transgenic plants with enhanced tolerance to environmental stress. Recently, in order to develop transgenic sweetpotato (tv. Yulmi) and potato (Solanum tuberosum L. cv. Atlantic and Superior) plants with enhanced tolerance to multiple stress, the genes of both CuZnSOD and APX were expressed in chloroplasts under the control of an SWPA2 promoter (referred to SSA plants). As expected, SSA sweetpotato and potato plants showed enhanced tolerance to methyl viologen-mediated oxidative stress. In addition, SSA plants showed enhanced tolerance to multiple stresses such as temperature stress, drought and sulphur dioxide. Our results strongly suggested that the rational manipulation of antioxidative mechanism in chloroplasts will be applicable to the development of all plant species with enhanced tolerance to multiple environmental stresses to contribute in solving the global food and environmental problems in the 21st century.

Ginsenoside F1 attenuates pirarubicin-induced cardiotoxicity by modulating Nrf2 and AKT/Bcl-2 signaling pathways

  • Yang Zhang;Jiulong Ma;Shan Liu;Chen Chen;Qi Li;Meng Qin;Liqun Ren
    • Journal of Ginseng Research
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    • 제47권1호
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    • pp.106-116
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    • 2023
  • Background: Pirarubicin (THP) is an anthracycline antibiotic used to treat various malignancies in humans. The clinical usefulness of THP is unfortunately limited by its dose-related cardiotoxicity. Ginsenoside F1 (GF1) is a metabolite formed when the ginsenosides Re and Rg1 are hydrolyzed. However, the protective effects and underlying mechanisms of GF1 on THP-induced cardiotoxicity remain unclear. Methods: We investigated the anti-apoptotic and anti-oxidative stress effects of GF1 on an in vitro model, using H9c2 cells stimulated by THP, plus trigonelline or AKT inhibitor imidazoquinoxaline (IMQ), as well as an in vivo model using THP-induced cardiotoxicity in rats. Using an enzyme-linked immunosorbent test, the levels of malondialdehyde (MDA), brain natriuretic peptide (BNP), creatine kinase (CK-MB), cardiac troponin (c-TnT), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione (GSH) were determined. Nuclear factor (erythroid-derived2)-like 2 (Nrf2) and the expression of Nrf2 target genes, including heme oxygenase-1 (HO-1), glutathione-S-transferase (Gst), glutamate-cysteine ligase modifier subunit (GCLM), and expression levels of AKT/Bcl-2 signaling pathway proteins were detected using Western blot analysis. Results: THP-induced myocardial histopathological damage, electrocardiogram (ECG) abnormalities, and cardiac dysfunction were reduced in vivo by GF1. GF1 also decreased MDA, BNP, CK-MB, c-TnT, and LDH levels in the serum, while raising SOD and GSH levels. GF1 boosted Nrf2 nuclear translocation and Nrf2 target gene expression, including HO-1, Gst, and GCLM. Furthermore, GF1 regulated apoptosis by activating AKT/Bcl-2 signaling pathways. Employing Nrf2 inhibitor trigonelline and AKT inhibitor IMQ revealed that GF1 lacked antioxidant and anti-apoptotic effects. Conclusion: In conclusion, GF1 was found to alleviate THP-induced cardiotoxicity via modulating Nrf2 and AKT/Bcl-2 signaling pathways, ultimately alleviating myocardial oxidative stress and apoptosis.

Effects of the NADPH Oxidase p22phox C242T Polymorphism on Endurance Exercise Performance and Oxidative DNA Damage in Response to Aerobic Exercise Training

  • Paik, Il-Young;Jin, Chan-Ho;Jin, Hwa-Eun;Kim, Young-Il;Cho, Su-Youn;Roh, Hee-Tae;Suh, Ah-Ram;Suh, Sang-Hoon
    • Molecules and Cells
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    • 제27권5호
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    • pp.557-562
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    • 2009
  • We examined the effects of the NADPH oxidase p22phox C242T polymorphism on endurance exercise performance and oxidative DNA damage in response to acute and chronic exercises. One hundred three subjects were recruited, among which 26 healthy subjects (CC: 12, TC: 12, and TT: 2) were studied during rest, exercise at 85% $VO_2max$, and recovery before and after 8 weeks of treadmill running. Lymphocyte DNA damage increased significantly in response to exercise (p < 0.05). There were no significant differences in plasma MDA, SOD concentrations and lymphocyte DNA damage between CC genotype and T allele group, but significant endurance training differences were observed. Endurance training increased exercise time to exhaustion in both the CC genotype and T allele groups (p < 0.05) but no significant difference was found between groups. The results of the current study with young, healthy, Korean men are interpreted to mean that 1) the majority had the CC genotype of the NADPH oxidase p22phox C242T polymorphism (82.5%: CC, 15.5%: TC, 1.9%: TT), 2) acute exercise increased lymphocyte DNA damage, 3) endurance training significantly increased exercise time to exhaustion, and alleviated lymphocyte DNA damage, and 4) The NADPH oxidase p22phox C242T polymorphism, however, did not alter lymphocyte DNA damage or exercise performance at rest, immediately after exercise, or during recovery.

인진청간탕(茵蔯淸肝湯)의 알코올성 산화스트레스에 대한 보호효과 연구 (Protective Effects of Yinjinchunggan-tang (YJCGT) on Alcohol-induced Oxidative Stress)

  • 김영태;우홍정
    • 대한한방내과학회지
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    • 제32권4호
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    • pp.550-564
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    • 2011
  • Objectives : Oxidative stress seems to play a major role in mechanisms by which ethanol causes liver injury. Previous studies have shown that treatment with Yinjinchunggan-tang (Yinchenqinggan-tang, YJCGT) has protective effects on alcoholic liver disease. The aim of this study was to investigate the protective effects of YJCGT on alcohol-induced oxidative stress. Materials and Methods : In vitro, we evaluated the inhibitory activities of YJCHT on DPPH(1,1-diphenyl-2-picryl-hydrazyl), xanthine oxidase, trypsin, and hyaluronidase. In a cell culture model, we measured cell viability and proliferation, and the activities of superoxide dismutase (SOD), and catalase (CAT) after YJCGT treatment in C34 and E47 cell lines, and HepG2 cells transfected with/ without cytochrome P450IIE1 (CYP2E1) gene. In vivo, we estimated serum level of hepatic biochemical markers, and alcohol concentration in the blood. Results : YJCGT showed significant free radical scavenging activity against DPPH and xanthine oxidase and decreased hyaluronidase activity effectively in vitro. YJCGT also increased cell viability, and proliferation in C34 and in E47 cell lines, and increased activities of superoxide dismutase, and catalase in C34 and in E47 cell lines. YJCGT reduced serum AST, LDH, and total cholesterol level in some of the results, and reduced blood alcohol concentration in vivo, as well. Conclusions : This study suggests that YJCGT has protective effects on oxidative stress by inhibiting alcohol-induced suppression of antioxidant enzyme activities.

Vascular Cell Responses against Oxidative Stress and its Application

  • Ryoo, Sung-Woo;Lee, Sang-Ki;Kim, Cuk-Seong;Jeon, Byeong-Hwa
    • International Journal of Vascular Biomedical Engineering
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    • 제2권2호
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    • pp.1-9
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    • 2004
  • The history of studies in biology regarding reactive oxygen species (ROS) is approximately 40 years. During the initial 30 years, it appeared that these studies were mainly focused on the toxicity of ROS. However, recent studies have identified another action regarding oxidative signaling, other than toxicity of ROS. Basically, it is suggested that ROS are reactive, and degenerate to biomolecules such as DNA and proteins, leading to deterioration of cellular functions as an oxidative stress. On the other hand, recent studies have shown that ROS act as oxidative signaling in cells, resulting in various gene expressions. Recently ROS emerged as critical signaling molecules in cardiovascular research. Several studies over the past decade have shown that physiological effects of vasoactive factors are mediated by these reactive species and, conversely, that altered redox mechanisms are implicated in the occurrence of metabolic and cardiovascular diseases ROS is a collective term often used by scientist to include not only the oxygen radicals($O2^{-{\cdot}},\;{^{\cdot}}OH$), but also some non-radical derivatives of oxygen. These include hydrogen peroxide, hypochlorous acid (HOCl) and ozone (O3). The superoxide anion ($O2^{-{\cdot}}$) is formed by the univalent reduction of triplet-state molecular oxygen ($^3O_2$). Superoxide dismutase (SOD)s convert superoxide enzymically into hydrogen peroxide. In biological tissues superoxide can also be converted nonenzymically into the nonradical species hydrogen peroxide and singlet oxygen ($^1O_2$). In the presence of reduced transition metals (e.g., ferrous or cuprous ions), hydrogen peroxide can be converted into the highly reactive hydroxyl radical (${^{\cdot}}OH$). Alternatively, hydrogen peroxide may be converted into water by the enzymes catalase or glutathione peroxidase. In the glutathione peroxidase reaction glutathione is oxidized to glutathione disulfide, which can be converted back to glutathione by glutathione reductase in an NADPH-consuming process.

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