• Title/Summary/Keyword: Protein pretreatment

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Hepatoprotective Activity of Fermented Curcuma longa L. on Galactosamine-Intoxicated Rats (발효울금의 갈락토사민 투여에 의한 흰쥐의 간독성에 대한 보효 효과)

  • Kim, Yong-Jae;You, Yang-Hee;Jun, Woo-Jin
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.41 no.6
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    • pp.790-795
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    • 2012
  • In this study, the general components and minerals of fermented Curcuma longa L. (FC) by Aspergillus oryzae were examined as well as the hepatoprotective effects of FC on acute hepatotoxicity induced by a single dose of galactosamine (GalN, 650 mg/kg body weight (b.w.)). The FC was found to consist of 0.15% moisture, 4.68% crude fat, 4.35% crude protein, 6.92% crude fiber, and 6.83% crude ash. The P, Ca, and Mg levels in FC were also quantitatively analyzed. Male Sprague-Dawley rats were divided into six groups; nontreated control, GalN, 150 mg/kg b.w. of silymarin plus GalN, 30 mg/kg b.w. of FC plus GalN, 100 mg/kg b.w. of FC plus GalN, and 300 mg/kg b.w. of FC plus GalN. Pretreatment 300 mg/kg b.w. of FC during 14 days significantly decreased the increased in aspartate aminotransferase, alanine amino transferase, and triglyceride (TG) induced by GalN. Severe liver damage, hepatocellular necrosis, infiltration of inflammatory cells, and councilman body necrosis on histopathological liver tissues were observed in GalN treated rats. Administration of 300 mg/kg b.w. of FC significantly decreased the degree of live damage. These results suggest that FC displays hepatoprotective activity and FC was able to lower the TG levels in serum; thus, FC may serve as a useful material for health food and clinical conditions associated with liver disease.

The Significance of Ku70 Expression in Patients with Nasopharyngeal Carcinoma (비인강암에서 방사선치료의 예측인자로써 Ku70 발현의 의의)

  • Song Si Yeol;Lee Sang-wook;Yu Eunsil;Cho Kyung-Ja;Park Jin-hong;Kim Sang Yoon;Nam Soon Yuhl;Lee Bong-Jae;Kim Sung Bae;Choi Seung-Ho;Ahn Seung Do;Shin Seong Soo;Choi Eun Kyung
    • Radiation Oncology Journal
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    • v.23 no.1
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    • pp.1-8
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    • 2005
  • Purpose : The objective of this study was to determine whether the expressions of the two components of DNA-dependent protein kinase, Ku70 and DNA-PKcs, influence the response to radiotherapy (RT) and outcome of treatment of non-disseminated nasopharyngeal carcinoma (NPC) in patients who received definitive RT. Materials and Methods : Sixty-six patients with NPC who were treated with radiotherapy alone or with concurrent chemotherapy between June 1995 and December 2001 were divided into groups based on the levels of immunoreactivity for Ku70 and DNA-PKcs in pretreatment biopsy specimens. The over-expression of Ku70 or DNA-PKcs groups Included patients whose biopsy specimens showed at least 50% immunopositive tumor cells; patients in which less than 50% of the tumor cells in the biopsy tissues were immunopositive were placed in the low Ku70 and DNA-PKcs groups. The immunoreactivities for Ku70 and DNA-PKcs were retrospectively compared with the sensitivity of the tumor to radiation and the patterns of therapy failure. Univariate analyses were peformed to determine the prognostic factors that influenced locoregional control of NPC. Results : The five-year locoregional control rate was significantly higher in the low Ku70 group (Ku(-)) (85%) than in the high Ku70 group (Ku(+)) (42%) (p=0.0042). However, there were no differences in the metastases-free survival rates between the two groups (Ku70 (+), 82%; Ku70 (-), 78%; p=0.8672). Univariate analysis indicated that the over-expression of Ku70 surpassed other well-known predictive clinocopathologic parameters as an Independent prognostic factor for locoregionai control. Eighteen of 22 patients who had locoregional recurrences of the tumor displayed an over-expression of Ku70. No significant association was found between the level of DNA-PKcs expression and the clinical outcome. Conclusion : Our data suggest that the level of Ku70 expression can be used as a molecular marker to predict the response to RT and the locoregional control after RT and concurrent chemotherapy in patients with non-disseminated NPC.

Activation of Pro-Apoptotic Multidomain Bcl-2 Family Member Bak and Mitochondria-Dependent Caspase Cascade are Involved in p-Coumaric Acid-Induced Apoptosis in Human Jurkat T Cells (p-Coumaric acid에 의해 유도되는 인체 Jurkat T 세포의 에폽토시스 기전)

  • Lee, Je-Won;Kim, Young-Ho
    • Journal of Life Science
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    • v.21 no.12
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    • pp.1678-1688
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    • 2011
  • The apoptogenic effect of p-coumaric acid, a phenolic acid found in various edible plants, on human acute leukemia Jurkat T cells was investigated. Exposure of Jurkat T cells to p-coumaric acid (50-$150{\mu}M$) caused cytotoxicity and TdT-mediated dUTP nick-end labeling (TUNEL)-positive apoptotic DNA fragmentation along with Bak activation, ${\Delta}{\psi}m$ loss, activation of caspase-9, -3, -7, and -8, and PARP degradation in a dose-dependent manner. However,these apoptotic events were completely abrogated in Jurkat T cells overexpressing Bcl-2.Under these conditions, necrosis was not accompanied. Pretreatment of the cells with the pan-caspase inhibitor (z-VAD-fmk) could prevent p-coumaric acid-induced sub-$G_1$ peak representing apoptotic cells, whereas it failed to block ${\Delta}{\psi}m$ loss, indicating that the activation of caspase cascade was prerequisite for p-coumaric acid-induced apoptosis as a downstream event of ${\Delta}{\psi}m$ loss. FADD- and caspase-8-positive wild-type Jurkat T cell clone A3, FADD-deficient Jurkat T cell clone I2.1, and caspase-8-deficient Jurkat T cell clone I9.2 exhibited similar susceptibilities to the cytotoxicity of p-coumaric acid, excluding an involvement of Fas/FasL system in triggering the apoptosis. The apoptogenic activity of p-coumaric acid is more potent in malignant Jurkat T cells than in normal human peripheral T cells. Together, these results demonstrated that p-coumaric acid-induced apoptogenic activity in Jurkat T cellswas mediated by Bak activation, ${\Delta}{\psi}m$ loss, and subsequent activation of multiple caspases such as caspase-9, -3, -7, and-8, and PARP degradation, which could be regulated by anti-apoptotic protein Bcl-2.

Ginsenoside compound K protects against cerebral ischemia/ reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

  • Qingxia Huang;Jing Li;Jinjin Chen;Zepeng Zhang;Peng Xu;Hongyu Qi;Zhaoqiang Chen;Jiaqi Liu;Jing Lu;Mengqi Shi;Yibin Zhang;Ying Ma;Daqing Zhao;Xiangyan Li
    • Journal of Ginseng Research
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    • v.47 no.3
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    • pp.408-419
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    • 2023
  • Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.

Effects of silage storage period of grass clippings on methane production by anaerobic digestion (잔디 예지물의 혐기소화에서 사일리지 저장기간이 메탄 생산에 미치는 영향)

  • Jin Yeo;Tae-Hee Kim;Chang-Gyu Kim;Seo-Yeong Lee;Young-Man Yoon
    • Journal of the Korea Organic Resources Recycling Association
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    • v.31 no.4
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    • pp.13-28
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    • 2023
  • This study assessed the biochemical methane potential (Bu-P) of three grass species-Poa pratensis (PP), Zoysia japonica (ZJ), and Agrostis stolonifera (AS). Bu-P values were determined as 0.330 Nm3/kg-VSadded for PP, 0.297 Nm3/kg-VSadded for ZJ, and 0.261 Nm3/kg-VSadded for AS. Notably, PP exhibited superior suitability for methane production. The investigation also examined the impact of silage storage duration on PP grass clippings, revealing a 19% decline in Bu-P from an initial value of 0.269 Nm3/kg-VSadded on day 0 to 0.217 Nm3/kg-VSadded on day 180. Throughout the storage period, there were significant increases in neutral detergent fiber (NDF), acid detergent fiber (ADF), and crude protein (CP) contents, rising from 67.59%, 39.68%, and 3.02% on day 0 to 77.12%, 54.65%, and 6.24% on day 180, respectively. These findings highlight the influence of storage duration on the anaerobic digestibility of PP grass clippings. To effectively utilize grass clippings as a renewable resource for methane production, further studies considering factors such as initial moisture content, pretreatment methods, and potential effects of residual pesticides are necessary to optimize anaerobic digestion efficiency for herbaceous biomass.

The Role of Poly(ADP-ribose) Polymerase-1 in Ventilator-Induced Lung Injury (기계환기로 인한 급성 폐손상에서 poly(ADP-ribose) polymerase-1의 역할)

  • Kim, Je-Hyeong;Yoon, Dae Wui;Hur, Gyu Young;Jung, Ki Hwan;Lee, Sung Yong;Lee, Sang Yeub;Shin, Chol;Shim, Jae Jeong;In, Kwang Ho;Yoo, Se Hwa;Kang, Kyung Ho
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.4
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    • pp.451-463
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    • 2006
  • Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.