• 제목/요약/키워드: Hydrogen Peroxide-induced Apoptosis

검색결과 136건 처리시간 0.042초

마늘성분 SAC 및 Hydrogen Peroxide에 의한 줄기세포의 유전자 발현 윤곽 (Gene Profile of Mesenchymal Stem Cell Induced by SAC or Hydrogen Peroxide (H2O2))

  • 박란숙
    • 한국식품영양학회지
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    • 제25권4호
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    • pp.863-870
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    • 2012
  • Though hydrogen peroxide ($H_2O_2$) causes a deleterious effect to cells with its reactive oxygen species resulting in cell death, S-allyl cysteine (SAC, a bioactive organosulfur compound of aged garlic extract) has been known to have a cytoprotective effect. Few reported profiles of gene expression of $H_2O_2$ and SAC treated human cord blood derived mesenchymal stem cells (MSC). This study revealed changes in the profile of twenty-one genes grouped by oxidative stress, antioxidant, cell death, anti-apoptosis and anti-aging by quantitative real time PCR. A concentration of $100{\mu}M$ of SAC or $50{\mu}M$ of $H_2O_2$ was applied to MSC which show moderate growth and apoptosis pattern. $H_2O_2$ treatment enhanced expression of eleven genes out of twenty-one genes compared with that of control group, on the contrary SAC suppressed expression of eighteen genes out of twenty-one genes except C ros oncogene. SAC decreased expression of oxidative stress genes such as SOD1, CAT and GPX. These results seemed consistent with reports which elucidated over-expression of NF-${\kappa}$B by $H_2O_2$, and suppression of it by SAC. This study will confer basic information for further experiments regarding the effects of SAC on gene levels.

Alpha-lipoic acid protects human dopaminergic neuronal cells against hydrogen peroxide-induced cell injury by inhibiting autophagy and apoptosis

  • Kang, Kyeong-Rok;Kim, Jae-Sung;Kim, Tae-Hyeon;Seo, Jeong-Yeon;Lim, HyangI;Park, Jong-Hyun;Yang, Kwang Yeol;Yu, Sun-Kyoung;Kim, Heung-Joong;Kim, Chun Sung;Chun, Hong Sung;Lee, Dong-Seol;Park, Joo-Cheol;Kim, Do Kyung
    • International Journal of Oral Biology
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    • 제46권1호
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    • pp.15-22
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    • 2021
  • Alpha-lipoic acid (ALA) is a naturally occurring antioxidant and has been previously used to treat diabetes and cardiovascular disease. However, the autophagy effects of ALA against oxidative stress-induced dopaminergic neuronal cell injury remain unclear. The aim of this study was to investigate the role of ALA in autophagy and apoptosis against oxidative stress in the SH-SY5Y human dopaminergic neuronal cell line. We examined SH-SY5Y phenotypes using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay (cell viability/proliferation), 4′,6-diamidino-2-phenylindole dihydrochloride nuclear staining, Live/Dead cell assay, cellular reactive oxygen species (ROS) assay, immunoblotting, and immunocytochemistry. Our data showed ALA attenuated hydrogen peroxide (H2O2)-induced ROS generation and cell death. ALA effectively suppressed Bax up-regulation and Bcl-2 and Bcl-xL down-regulation. Furthermore, ALA increased the expression of the antioxidant enzyme, heme oxygenase-1. Moreover, the expression of Beclin-1 and LC-3 autophagy biomarkers was decreased by ALA in our cell model. Combined, these data suggest ALA protects human dopaminergic neuronal cells against H2O2-induced cell injury by inhibiting autophagy and apoptosis.

15-DEOXY-$\Delta^{12,14}$ PROSTAGLANDIN $\textrm{J}_2$ RESCUES PC12 CELLS FROM HYDROGEN PEROXIDE-INDUCED APOPTOSIS THROUGH POTENTIATION OF CELLULAR ANTIOXIDATIVE DEFENSE CAPACITY

  • Kim, Ji-Woo;Jang, Jung-Hee;Surh, Young-Joon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2003년도 춘계학술대회 논문집
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    • pp.91-92
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    • 2003
  • Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O$$_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. (omitted)

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15-DEoxy-$d^{12,14}$ Prostaglandin $J_2$ Rescues Pc12 Cells From Hydrogen Peroxide-induced Apoptosis Through Upregulation Of Heme Oxygenase-1

  • Kim, Ji-Woo;Jang, Jung-Hee;Surh, Young-Joon
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.153.1-153.1
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    • 2003
  • Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. l5-Deoxy-$D^{12, 14}$ prostaglandin $J_2$ (15d-$PGJ_2$), a dehydration product of prostaglandin $D_2$, has been reportd to possess a number of biological activities such as anti-inflammatory, anticarcinogenic, and antioxidative properties. (omitted)

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Quercetin Prevents Hydrogen Peroxide-induced Necrotic and Apoptotic Cell Death in Human Colonic Epithelial Cells

  • Jung, Soon-Hee
    • 대한임상검사과학회지
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    • 제43권4호
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    • pp.161-170
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    • 2011
  • Quercetin is one of the most distributed flavonoids in the plant kingdom and occurs naturally in a wide range of fruits and vegetables. This study was undertaken to determine whether quercetin exerts beneficial effect against necrotic and apoptotic cell death induced by hydrogen peroxide ($H_2O2$) in intestinal cells using the human-derived cultured T84 colonic epithelial cell line. Necrotic cell death was induced by exposing cells to 0.5 mM $H_2O_2$ for 2 h and apoptosis was induced by incubating cells in normal culture medium for 18 h following exposure of cells to 0.5 mM $H_2O2$ for 2 h. Cell viability was evaluated by the trypan blue exclusion assay and apoptosis was assessed by Hoechst 33258 staining and flow cytometry. $H_2O_2$ induced necrotic cell death in a time and dose-dependent fashion. Both necrotic and apoptotic cell deaths were not prevented by the antioxidants N,N'-diphenyl-p-phenylenediamine(DPPD) and Trolox, whereas both cell deaths induced by the organic hydroperoxide t-butylhydroperoxide (tBHP) were prevented by DPPD, suggesting that $H_2O_2$ induces cell death through a lipid peroxidation-independent mechanism. $H_2O2$-induced necrotic death was prevented by deferoxamine and 3-aminobenzamide, while the apoptotic cell death was not affected by these agents. Quercetin prevented both necrotic and apoptotic cell deaths induced by $H_2O_2$ in a dose-dependent manner. $H_2O_2$ caused activation of poly (ADP-ribose) polmerase (PARP), which was inhibited by deferoxamine, 3-aminobenzamide, and quercetin, but not DPPD. These results indicate that quercetin inhibits both necroticand apoptotic deaths of T84 cells. The anti-necrotic effect of quercetin may be attributed to its iron chelator activity rather than a direct $H_2O_2$ scavenging capacity and antioxidant. The present study suggests that quercetin may play a therapeutic role in the treatment of human gastrointestinal diseases mediated by oxidants.

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C2C12 근아세포에서 산자나무 유래 Isorhamnetin의 산화적 스트레스에 의한 Apoptosis 유발 억제 효과 (Protective Effects of Isorhamnetin against Hydrogen Peroxide-Induced Apoptosis in C2C12 Murine Myoblasts)

  • 최영현
    • 한방비만학회지
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    • 제15권2호
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    • pp.93-103
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    • 2015
  • Objectives: It was investigated the cytoprotective efficacies of isorhamnetin, a flavonoid originally derived from Hippophae rhamnoides L., against oxidative stress-induced apoptosis in C2C12 myoblasts. Methods: The effects of isorhamnetin on cell growth, apoptosis and reactive oxygen species (ROS) generation were evaluated by trypan blue dye exclusion assay, 4',6-diamidino-2-phenylindole staining and flow cytometry. The levels of apoptosis-regulatory and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway-related proteins, and caspase activities (caspase-3 and -9) were determined by Western blot analysis and colorimetric assay, respectively. Results: Our results revealed that treatment with isorhamnetin prior to hydrogen peroxide ($H_2O_2$) exposure significantly increased the C2C12 cell viability and, indicating that the exposure of C2C12 cells to isorhamnetin conferred a protective effect against oxidative stress. Isorhamnetin also effectively attenuated $H_2O_2$-induced apoptosis and ROS generation, which was associated with the restoration of the upregulation of Bax and downregulation of Bcl-2 induced by $H_2O_2$. In addition, $H_2O_2$ enhanced the activation of caspase-9 and -3, and degradation of poly (ADP-ribose)-polymerase, a typical substrate protein of activated caspase-3; however, these events were almost totally reversed by pretreatment with isorhamnetin. Moreover, isorhamnetin increased the levels of heme oxygenase-1, a potent antioxidant enzyme, associated with the induction of Nrf2. Conclusions: Our data indicated that isorhamnetin may potentially serve as an agent for the treatment and prevention of muscle disorders caused by oxidative stress.

miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase

  • Long, Bo;Gan, Tian-Yi;Zhang, Rong-Cheng;Zhang, Yu-Hui
    • Molecules and Cells
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    • 제40권8호
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    • pp.542-549
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    • 2017
  • Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.

Antioxidants May Protect Cancer Cells from Apoptosis Signals and Enhance Cell Viability

  • Akan, Zafer;Garip, Ayse Inhan
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권8호
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    • pp.4611-4614
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    • 2013
  • Quercetin is one of the most abundant dietary flavonoids widely present in many fruits and vegetables. Previous in vitro studies has shown that quercetin acts as an antioxidant and anti-inflammatory agent and it has potent anticarcinogenic properties as an apoptosis inducer. In this study we examined apoptotic effects of quercetin on the K562 erythroleukemia cell line. K562 cells were induced to undergo apoptosis by hydrogen peroxide. Cell viability and apoptosis level were assessed by annexin V and PI staining methods using flow cytometry. Viability of K562 cells was increased by low dose of quercetin (5-100 ${\mu}M$) for 3 hours. High doses of quercetin proved toxic (100-500 ${\mu}M$, 24 hours) and resulted in decrease of K562 cell viability as expected (p<0.01). As to results, 100 ${\mu}M$ quercetin was defined as a protective dose. Also, K562 cell apoptosis due to hydrogen peroxide was decreased in a dose dependent manner. As indicated in previous studies, reduction of superoxides by free radical scavengers like quercetin could be beneficial for prevention of cancer but consumption of such flavonoids during cancer treatment may weaken effects of chemotherapeutics and radiotherapy. Especially cancer patients should be carefully considered for traditional phytotherapy during cancer treatment, which can lead to controversial results.

내독소로 자극된 당뇨환자의 중성구에서 기획성 세포사멸과 과산화수소 분비능 (Neutrophil Apoptosis and $H_2O_2$ Release by LPS in Diabetics)

  • 서기현;나주옥;문승혁;어수택;김용훈;박춘식
    • Tuberculosis and Respiratory Diseases
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    • 제57권3호
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    • pp.250-256
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    • 2004
  • 배 경 : 세균 감염 시 이환율과 사망률이 증가한다고 알려져 있는 당뇨에서 염증 조직 내 활성 산소 기능과 세균능 감소를 보이는 중성구의 기능 이상이 잘 알려져 있다. 또한, 기획성 세포사멸이 중성구 제거에 중요한 역할을 한다고 알려져 있다. 중성구의 기획성 세포사멸은 염증 조직 내I 균형을 유지하는 데 중요하다. 실제 당뇨병에서 중성구의 기획성 세포사멸과 활성 산소에 대한 연구가 없는 실정으로 본 연구를 통해 당뇨에서 내독소 투여시 중성구의 기획성 세포사멸과 과산화수소 분비능을 알고자 하였다. 방 법 : 정상과 당뇨 환자의 전혈을 뽑아 중성구 만을 추출하여 내독소에 노출시킨 후 중성구의 기획성 세포사멸, 과산화수소 분비능, 생존율을 각각 측정하였다. 결 과 : 정상 중성구는 내독소 투여 후 기획성 세포사멸이 감소하는 경향을 보였다. 정상과 비교할 때 당뇨환자의 중성구는 기획성 세포사멸이 감소하였고 특히 내 독소를 투여한 군에서 더욱 감소하였다. 과산화수소 분비능의 차이는 보이지 않았다. 결 론 : 본 연구를 통해 당뇨환자에서 내독소 투여로 인한 중성구의 기획성 세포사멸 감소가 당뇨에서 중증 감염과 높은 사망률에 영향을 줄 것으로 사료된다.

가감당귀음자의 항산화 효과와 자외선으로 유도된 각질형성세포 손상에 대한 보호효과 (Antioxidant and Protective Effects of Gagam-Danguieumja on Ultraviolet B-induced Damage in Human Keratinocytes)

  • 김태연;박종필
    • 동의생리병리학회지
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    • 제29권6호
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    • pp.475-484
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    • 2015
  • In this paper, we studied the anti-oxidative capacities and protective effects of water extract of Gagam-Danguieumja(GDE) against Ultraviolet B(UVB)-induced oxidative damage in human keratinocytes(HaCaT). To evaluate the anti-oxidative activities of GDE, we measured scavenging activities on DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion, lipid peroxidation and reducing power of GDE. To detect the protective effects of GDE against UVB, we irradiated with 40 mJ/㎠`s UVB to HaCaT cells then we measured reactive oxygen species(ROS) generation, apoptotic bodies and cell viability using DCFH-DA assay, Hoechst 33342 staining and MTT assay. GDE showed the anti-oxidative activities by scavenging DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion, lipid peroxidation. Also GDE showed high reducing values. GDE reduced oxidative stress conditions by inhibition of ROS expression. Also the cell apoptosis by UVB-induced oxidative conditions was decreased by GDE treatment. These results could suggest that GDE had anti-oxidative activities and exhibited protective effects against UVB on HaCaT cells. GDE would be useful for the development of cosmetics treating UVB-induced skin aging.