• 제목/요약/키워드: Protective agents

검색결과 278건 처리시간 0.023초

자율적응형 과전류계전기 에이전트의 통신을 위한 ACL모듈 개발 (Development of ACL Modul For Agent Communication in Auto-Adaptive OCR Agent)

  • 오태욱;이승재;최면송;김기화;임성일;민병운;이한웅
    • 대한전기학회:학술대회논문집
    • /
    • 대한전기학회 2002년도 하계학술대회 논문집 A
    • /
    • pp.193-195
    • /
    • 2002
  • In this paper, a communication module is proposed to be applied to communication between over current relay (OCR) agents in multi agent protection system. A multi agent system can achieve a global goal beyond the ability of each individual agent by working together, in which it is the prerequisite for each agent to be able to exchange or share information or processing status with other agent. The proposed communication module is purposed to enable not only each agent to bring about its own goal, but also the whole protective system to provide much improved coordinated protection. It is applied to a self adaptive protection system for a distribution network using multi agent concept to show its effectiveness.

  • PDF

Heme Oxygenase-1 as a Potential Therapeutic Target for Hepatoprotection

  • Farombi, Ebenezer Olatunde;Surh, Young-Joon
    • BMB Reports
    • /
    • 제39권5호
    • /
    • pp.479-491
    • /
    • 2006
  • Heme oxygenase (HO), the rate limiting enzyme in the breakdown of heme into carbon monoxide (CO), iron and bilirubin, has recently received overwhelming research attention. To date three mammalian HO isozymes have been identified, and the only inducible form is HO-1 while HO-2 and HO-3 are constitutively expressed. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-${\kappa}B$) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. The products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect against chemically-induced liver injury as well as hepatocarcinogenesis.

An Additional Mechanism for the Cytotoxicity of 2-Chloroethylethyl Sulfide in Spleen Lymphocytes; Lysosomal Labilization

  • Choi, Dae-Sung;Shin, Sung-Ho;Kim, Yun-Bae;Cha, Seung-Hee;Sok, Dai-Eun
    • BMB Reports
    • /
    • 제28권1호
    • /
    • pp.79-82
    • /
    • 1995
  • Exposure of spleen lymphocytes to 2-chloroethylethyl sulfide (CEES) leads to a reduction of the intracellular ATP level, followed by a decrease in cell viability. Addition of nicotinamide, an inhibitor of poly(ADP-ribose) polymerase (PADPRP), restores both ATP level and viability, indicating that an activation of PADPRP is responsible for the cytotoxicity of CEES. The involvement of a $Ca^{2+}$-mediated process in cytotoxicity is suggested. Verapamil, EGTA, trifluoperazine, and butacaine exhibit a partial protection (20 to 58%) against the cytotoxicity of CEES. Investigation of the causative role of proteolytic degradation in cell death indicate that pepstatin and leupeptin exert a substantial protective effect (60 to 70%), suggesting the involvement of lysosomal destabilization in CEES-induced cytotoxicity. Also, lysosomotropic agents markedly decrease the cytotoxicity. Lysosomal labilization may be a mechanism for the cytotoxicity of CEES.

  • PDF

Implications of NQO1 in cancer therapy

  • Oh, Eun-Taex;Park, Heon Joo
    • BMB Reports
    • /
    • 제48권11호
    • /
    • pp.609-617
    • /
    • 2015
  • NAD(P)H:quinone oxidoreductase (NQO1), an obligatory two-electron reductase, is a ubiquitous cytosolic enzyme that catalyzes the reduction of quinone substrates. The NQO1- mediated two-electron reduction of quinones can be either chemoprotection/detoxification or a chemotherapeutic response, depending on the target quinones. When toxic quinones are reduced by NQO1, they are conjugated with glutathione or glucuronic acid and excreted from the cells. Based on this protective effect of NQO1, the use of dietary compounds to induce the expression of NQO1 has emerged as a promising strategy for cancer prevention. On the other hand, NQO1-mediated two-electron reduction converts certain quinone compounds (such as mitomycin C, E09, RH1 and β-lapachone) to cytotoxic agents, leading to cell death. It has been known that NQO1 is expressed at high levels in numerous human cancers, including breast, colon, cervix, lung, and pancreas, as compared with normal tissues. This implies that tumors can be preferentially damaged relative to normal tissue by cytotoxic quinone drugs. Importantly, NQO1 has been shown to stabilize many proteins, including p53 and p33ING1b, by inhibiting their proteasomal degradation. This review will summarize the biological roles of NQO1 in cancer, with emphasis on recent findings and the potential of NQO1 as a therapeutic target for the cancer therapy.

Grapefruit Juice Suppresses Azoxymethane-induced Colon Aberrant Crypt Formation and Induces Antioxidant Capacity in Mice

  • Madrigal-Bujaidar, Eduardo;Roaro, Laura Martino;Garcia-Aguirre, Karol;Garcia-Medina, Sandra;Alvarez-Gonzalez, Isela
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제14권11호
    • /
    • pp.6851-6856
    • /
    • 2013
  • In the present report we determined the protective capacity of grapefruit juice (GJ) against molecular and cellular damage in azoxymethane (AOM) treated mice. Animals were daily administered GJ orally (0.8, 4.1, and 8.2 ${\mu}l/g$) for seven weeks, as well as intraperitoneally (ip) injected with AOM twice (weeks 2 and 3 of the assay). Control groups administered with water, with the high dose of GJ, and with AOM injected in weeks 2 and 3 were also included. The results showed a significant, dose-dependent protection of GJ on the number of colon aberrant crypts (AC) induced by AOM. The highest inhibitory effect was reached with the highest tested dose of GJ, decreasing ACF by 51% and 43% at weeks 4 and 7 of the assay. Regarding protein and lipid oxidation we also found a dose-dependent decrease caused with GJ in comparison with the increased levels produced by AOM. Therefore, our results established chemopreventive potential for GJ, and suggested effects related to its antioxidant capacity. Finally, we found that the tested agents induced neither micronuclei increase nor alteration in bone marrow cytotoxicity.

B16F10 Murine Melanoma 세포에서 멜라닌생성억제에 대한 타우린의 효과 (Antimelanogenic Effect of Taurine in Murine Melanoma B16F10 Cells)

  • 정효숙;송경희;김안근
    • 약학회지
    • /
    • 제51권5호
    • /
    • pp.350-354
    • /
    • 2007
  • Taurine has been shown to be tissue-protective against oxidant-induced injury and is a powerful regulator of the immune system. However, there is no study on the antimelanogenic effect of taurine. In this study, we investigated the whitening effect of taurine in B16F10 mouse melanoma cells. Cell viability was measured by MTT assay. We examined melanin contents and tyrosinase activity according to time and concentration. Extracellular signal regulated kinase (ERK) is an important regulator of melanogenesis. It has been reported that activated ERK induced microphthalmia associated transcription factor (MITF) phosphorylation and its subsequent degradation and thus reduced melanin synthesis. In our B16F10 cell culture system, taurine led to decrease melanin contents by 21% at 48 hr. We then observed taurine effects on ERK-P, MITF and tyrosinase by Western blot. ERK was activated at 18 hr and 24 hr, whereas MITF reduced. We could not observe any differences in the levels of tyrosinase. These results suggested that taurine inhibited melanogenesis by ERK signal pathway via MITF degradation. We expect that taurine has potential skin whitening agents in cosmetics.

유제품의 치매 및 인지기능 저하 예방 효과 (Preventive Effects of Dairy Products on Dementia and Cognitive Decline)

  • 윤정희;설국환;유자연;오미화;함준상
    • Journal of Dairy Science and Biotechnology
    • /
    • 제38권1호
    • /
    • pp.27-36
    • /
    • 2020
  • The prevention of cognitive decline and dementia is an increasingly important global public health priority due to an increase in the percentage of the elderly population. Dementia, a severe cognitive disorder, not only negatively impacts the patients' quality of life but also creates a substantial burden for caregivers. This review introduced recent advances regarding the protective effects of dairy product intake against dementia and cognitive decline. Recent epidemiological studies have suggested that specific components of dairy products including bioactive peptides, colostrinin, proline-rich polypeptides, α-lactalbumin, vitamin B12, calcium, and probiotics might promote healthy brain function during aging. Additionally, oleamide and dehydroergosterol in Camembert cheese have been suggested as agents capable of reducing microglial inflammatory responses and neurotoxicity. The intake of neuroprotective and anti-inflammatory compounds in meals is safe and easy, hence nutritional approaches, including dairy product consumption, serve as a promising intervention for the prevention of neurodegenerative disorders.

Iridoid 화합물이 창상 치유에 미치는 영향 (The Effects of Iridoid Compounds on Wound Healing)

  • 이승우;고홍섭;이상구
    • Journal of Oral Medicine and Pain
    • /
    • 제24권2호
    • /
    • pp.137-143
    • /
    • 1999
  • Aucubin, the natural product, which is isolated from Aucuba japonica, has a variety of pharmacological effects such as liver-protective function, inhibition of liver RNA and protein biosynthesis, hypotensive activity and antimicrobial effect, etc. This study was performed to investigate the effects of iridoid compounds on wound healing. The author prepared 0.1% aucubin solution and 0.1% aucubin ointment as an active form, aucubigenin to which aucubin was converted by ${\beta}$-glucosidase. Artificial surgical wound was made on either 1cm lateral side of the dorsal midline along the axis of spine of Sprague-Dawley rats under sterile technique. Application of 0.1% aucubin solution or 0.1% aucubin ointment to surgical wound was done daily. Light microscopic examination was performed on the postsurgical 3 days, 5 days, and 9 days. The 0.1% aucubin solution group epithelialized earlier than the control group and the fibrosis of granulation tissue of both aucubin groups were more prominent than the control group. Collectively, this study suggests the possibility of aucubin as a topical agent. Further research should be performed on the mechanism of aucubin on wound healing and proper formulation for effective topical agents.

  • PDF

방사선의 발생독성 검색을 위한 단기 최기형성 시험법의 확립 (Establishment of Short-Term Teratogenicity Study for Detecting Developmental Toxicity Induced by Gamma Radiation)

  • 김종춘;김성호;신동호;신진영;김세라;이해준;박승춘;조성기;이윤실
    • Toxicological Research
    • /
    • 제20권2호
    • /
    • pp.117-122
    • /
    • 2004
  • The present study was carried out to establish a short-term teratogenicity study for detecting developmental toxic potential induced by gamma radiation in ICR mice. Pregnant mice were exposed at dose levels of 0, 0.5, 1, 2, or 4 Gy on gestational day 8.5. All dams were subjected to caesarean section on gestational day 10.5 and their embryos were examined for growth, differentiation, and morphological abnormalities. An increase in the number of resorption was found at 4 Gy in a dose-dependent manner. Dose-dependent decreases in the developmental score of yolk sac circulation and olfactory system at above 1 Gy, in the number of somite pairs and developmental score of allantois, optic system, and maxillary process at above 2 Gy, and in the all growth and developmental parameters examined at 4 Gy were found. Various types of morphological abnormalities were seen at dose levels of 0.5 Gy or greater. Characteristic malformations induced by gamma radiation were abnormal axial rotation, hematoma, craniofacial hypoplasia, open neuropore, shortened prosencephalon, kinked somites, irregular somites, swelling, hydropericardium, absent branchial bar, and absent limb bud. Morphological alterations such as hematoma, craniofacial hypoplasia, open neuropore, and kinked somites were noted even in the lowest dose (0.5 Gy). These results indicated that the short-term teratogenicity study established in this study can be a useful tool for not only detecting the developmental toxic potential induced by gamma radiation, but also screening radio-protective agents in ICR mice.

활성산소 소거활성에 따른 꾸지뽕잎 추출물의 신경세포 보호 효과 (Neuroprotective Effect according to Reactive Oxygen Species Scavenging Activity from Extracts of Cudrania tricuspidata Leaves)

  • 강용경;이은아;박해룡
    • 한국식품조리과학회지
    • /
    • 제28권6호
    • /
    • pp.821-828
    • /
    • 2012
  • In an attempt to identify the neuroprotective effect of Cudrania tricuspidata (CT) leaves against ROS (reactive oxygen species)-induced oxidative stress in neuronal cells, the extracts from CT leaves were investigated using PC12 cells and N18-RE-105 cells. The methanolic and ethanolic extracts from CT were denoted as CTM (Cudrania tricuspidata Leaves methanolic extracts) and CTE (Cudrania tricuspidata Leaves ethanolic extracts), respectively. The neuroprotective effects of the extracts were measured by DCF-DA assay, MTT reduction assay, and LDH release assay. The PC12 cells exposed to $H_2O_2$-induced oxidative stress and the N18-RE-105 cells exposed to glutamate-induced oxidative stress were treated with various concentrations of CTM and CTE. The results, CTM treatments resulted in the induction of a dose-dependent protective effect in PC12 cells and N18-RE-105 cells. Interestingly, CTE also showed neuroprotective effect in PC12 cells and N18-RE-105 cells. Therefore, these results suggest that CTM and CTE could be a new potential candidate as neuroprotective agents against ROS-induced oxidative stress in neuronal cells.