• Title/Summary/Keyword: Animal disease model

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Expression of Antisense Mouse Obese Gene in Transgenic Mice (형질전환 생쥐에서 Antisense 비만유전자의 발현)

  • Kwon, B.S.;Hong, K.H.;Jahng, J.W.;Lee, H.T.;Chung, K.S.
    • Korean Journal of Animal Reproduction
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    • v.24 no.4
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    • pp.419-428
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    • 2000
  • Leptin, the product of obese (ob) gene, is an adipocyte-derived satiety factor that plays a major role in the regulation of food intake, energy homeostasis, body weight, reproductive physiology and neuropeptide secretion. The present study was designed to generate transgenic mice expressing antisense mouse ob (mob) gene. Total RNA was extracted from the adipose tissues of mouse, then reverse transcription was performed. The 303 and 635 bp fragments of anti I and II cDNAs were amplified from mob cDNAs by PCR. The two mob cDNAs were reversely ligated into between adipose tissue specific aP2 promote and SV40 poly(A) site. Transgenic mice carrying two different kinds of antisense mob transgenes were generated by DNA microinjection into pronucleus. Total 14 transgenic mice were born, and the 4 and 5 founder lines of the transgenic mice with anti I and II transgenes were respectively established. Antisense mRNA expression was detected in transgenic F$_1$ mice by RT-PCR analysis. This result suggests that the transgenic mice expressing antisense mob mRNA may be useful as an animal disease model to be obesity caused by decreased amount of leptin secretion.

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Study on the Methodology of the Microbial Risk Assessment in Food (식품중 미생물 위해성평가 방법론 연구)

  • 이효민;최시내;윤은경;한지연;김창민;김길생
    • Journal of Food Hygiene and Safety
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    • v.14 no.4
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    • pp.319-326
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    • 1999
  • Recently, it is continuously rising to concern about the health risk being induced by microorganisms in food such as Escherichia coli O157:H7 and Listeria monocytogenes. Various organizations and regulatory agencies including U.S.FPA, U.S.DA and FAO/WHO are preparing the methodology building to apply microbial quantitative risk assessment to risk-based food safety program. Microbial risks are primarily the result of single exposure and its health impacts are immediate and serious. Therefore, the methodology of risk assessment differs from that of chemical risk assessment. Microbial quantitative risk assessment consists of tow steps; hazard identification, exposure assessment, dose-response assessment and risk characterization. Hazard identification is accomplished by observing and defining the types of adverse health effects in humans associated with exposure to foodborne agents. Epidemiological evidence which links the various disease with the particular exposure route is an important component of this identification. Exposure assessment includes the quantification of microbial exposure regarding the dynamics of microbial growth in food processing, transport, packaging and specific time-temperature conditions at various points from animal production to consumption. Dose-response assessment is the process characterizing dose-response correlation between microbial exposure and disease incidence. Unlike chemical carcinogens, the dose-response assessment for microbial pathogens has not focused on animal models for extrapolation to humans. Risk characterization links the exposure assessment and dose-response assessment and involve uncertainty analysis. The methodology of microbial dose-response assessment is classified as nonthreshold and thresh-old approach. The nonthreshold model have assumption that one organism is capable of producing an infection if it arrives at an appropriate site and organism have independence. Recently, the Exponential, Beta-poission, Gompertz, and Gamma-weibull models are using as nonthreshold model. The Log-normal and Log-logistic models are using as threshold model. The threshold has the assumption that a toxicant is produce by interaction of organisms. In this study, it was reviewed detailed process including risk value using model parameter and microbial exposure dose. Also this study suggested model application methodology in field of exposure assessment using assumed food microbial data(NaCl, water activity, temperature, pH, etc.) and the commercially used Food MicroModel. We recognized that human volunteer data to the healthy man are preferred rather than epidemiological data fur obtaining exact dose-response data. But, the foreign agencies are studying the characterization of correlation between human and animal. For the comparison of differences to the population sensitivity: it must be executed domestic study such as the establishment of dose-response data to the Korean volunteer by each microbial and microbial exposure assessment in food.

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A Study on U-Livestock Integrated Service on Ubiquitous Technologies (유비쿼터스 기술을 활용한 축산부문 U-축산 융합서비스 도입연구)

  • Koo, J.H.;Jung, T.W.;Lee, S.R.
    • Journal of Animal Environmental Science
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    • v.18 no.1
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    • pp.9-18
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    • 2012
  • The output of Korea's livestock industry represents about 40% of the total agricultural production, making it the most high value-added sector in the entire agricultural and forestry industry. However, the fatal epidemics such as foot-and-mouth disease and avian influenza spurs demands for the advanced management of livestock production with IT technologies. U-Livestock means the application of ubiquitous technologies to livestock production. In this study, U-Livestock service models are established on the basis of the life cycle of livestock by using local and overseas cases. The objectives, contents, and structures of service models are required to be designed in detail respectively. The integration of such service models is expected to he1p modernize the livestock industry and raise the productivity of sector.

Comparison of the presentation of atopic dermatitis induced by trinitrochlorobenzene and house dust mite in NC/Nga mice

  • Kim, Yoon-Hwan;Kim, Tae Hyeong;Kang, Min Soo;Ahn, Jin-Ok;Choi, Jung Hoon;Chung, Jin-Young
    • Journal of Veterinary Science
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    • v.21 no.4
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    • pp.59.1-59.12
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    • 2020
  • Background: Atopic dermatitis (AD) is a common chronic inflammatory skin disease. To understand AD, there have been many trials establishing AD animal models. Although various trials to establish AD animal models have been existed, even the mechanisms of AD in animal models are not enough clarified. Objectives: This study assessed AD characteristics induced in Nishiki-nezumi Cinnamon/Nagoya (Nc/Nga) mice following trinitrochlorobenzene (TNCB) treatment for different periods and house dust mite (HDM) treatment to compare each model's immunological patterns, especially with cytokine antibody array tool. Methods: In this study, we exposed Nc/Nga mice to TNCB or HDM extract to induce AD. Nc/Nga mice were divided into 4 groups: control, TNCB 2 weeks-treated, TNCB 8 weeks-treated, and HDM-treated groups. After AD induction, all mice were evaluated by serum immunoglobulin E (IgE) concentration and serum cytokine antibody assays, scoring of skin lesions, scoring of scratching frequency, and histological analysis. Results: The results showed significant differences between groups in serum IgE concentration, skin lesion scores, and scratching frequency. The analysis results for serum cytokine antibody arrays showed that in the TNCB 8 weeks- and HDM-treated groups, but not in the TNCB 2 weeks-treated group, expressions of genes related to the immune response were enriched. Among the histological results, the skin lesions in the HDM-treated group were most similar to those of AD. Conclusions: We confirmed that immunological pattern of AD mice was markedly different between HDM and TNCB treated groups. In addition, the immunological pattern was quietly different dependent on TNCB treated duration.

The Slough of Cicadidae Periostracum Ameliorated Lichenification by Inhibiting Interleukin (IL)-22/Janus Kinase (JAK) 1/Signal Transducer and Activator of Transcription (STAT) 3 Pathway in Atopic Dermatitis

  • Ganghye Park;Namgyu Kwon;Mi Hye Kim;Woong Mo Yang
    • Food Science of Animal Resources
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    • v.43 no.5
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    • pp.859-876
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    • 2023
  • It is known that animal-origin medicine could be one of effective treatment to remedy atopic dermatitis (AD) by controlling the cytokines. Cicadidae Periostracum (CP), the slough of Cryptotympana pustulata, has been frequently used for treating AD and skin affliction in traditional Korean Medicine. This study is aimed at investigating the ameliorating effects of CP on AD and its potential mechanism. The dinitrochlorobenzene sensitized mice were treated with CP for 2 weeks. The various biomarkers and the dermatitis scores presented that CP treatment can induce the visual and biological improvements of AD model. Pruritus, the most serious symptom of AD, which can cause repeated scratching behaviors and finally lead to lichenification, was reduced with CP treatment by regulating the inflammatory reactions. In addition, CP treatment diminished the number of mast cells that are known for causing inflammatory reactions. Moreover, it is proven that CP can decline secretion of interleukin-22, which means CP treatment has anti-inflammatory effects. CP treatment can correct the imbalance of helper T (Th)1 and Th2, downregulating thymic stromal lymphopoietin that leads to decrease of mRNA level of inflammatory cytokines. The crucial role of CP treatment is controlling of the Janus kinase 1/signal transducer and activator of transcription 3 pathway. In addition, CP treatment has the inhibitory effects on kallikrein related peptidase (KLK) 5 and KLK7. Taken together, CP treatment can ameliorate most symptoms and problems caused by AD disease, improving the AD patients' life quality.

Multitarget effects of Korean Red Ginseng in animal model of Parkinson's disease: antiapoptosis, antioxidant, antiinflammation, and maintenance of blood-brain barrier integrity

  • Choi, Jong Hee;Jang, Minhee;Nah, Seung-Yeol;Oh, Seikwan;Cho, Ik-Hyun
    • Journal of Ginseng Research
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    • v.42 no.3
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    • pp.379-388
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    • 2018
  • Background: Ginsenosides are the main ingredients of Korean Red Ginseng. They have extensively been studied for their beneficial value in neurodegenerative diseases such as Parkinson's disease (PD). However, the multitarget effects of Korean Red Ginseng extract (KRGE) with various components are unclear. Methods: We investigated the multitarget activities of KRGE on neurological dysfunction and neurotoxicity in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. KRGE (37.5 mg/ kg/day, 75 mg/kg/day, or 150 mg/kg/day, per os (p.o.)) was given daily before or after MPTP intoxication. Results: Pretreatment with 150 mg/kg/day KRGE produced the greatest positive effect on motor dysfunction as assessed using rotarod, pole, and nesting tests, and on the survival rate. KRGE displayed a wide therapeutic time window. These effects were related to reductions in the loss of tyrosine hydroxylase-immunoreactive dopaminergic neurons, apoptosis, microglial activation, and activation of inflammatory factors in the substantia nigra pars compacta and/or striatum after MPTP intoxication. In addition, pretreatment with KRGE activated the nuclear factor erythroid 2-related factor 2 pathways and inhibited phosphorylation of the mitogen-activated protein kinases and nuclear factor-kappa B signaling pathways, as well as blocked the alteration of blood-brain barrier integrity. Conclusion: These results suggest that KRGE may effectively reduce MPTP-induced neurotoxicity with a wide therapeutic time window through multitarget effects including antiapoptosis, antiinflammation, antioxidant, and maintenance of blood-brain barrier integrity. KRGE has potential as a multitarget drug or functional food for safe preventive and therapeutic strategies for PD.

Gintonin, a Panax ginseng-derived LPA receptor ligand, attenuates kainic acid-induced seizures and neuronal cell death in the hippocampus via anti-inflammatory and anti-oxidant activities

  • Jong Hee Choi;Tae Woo Kwon;Hyo Sung Jo;Yujeong Ha;Ik-Hyun Cho
    • Journal of Ginseng Research
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    • v.47 no.3
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    • pp.390-399
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    • 2023
  • Background: Gintonin (GT), a Panax ginseng-derived lysophosphatidic acid receptor (LPAR) ligand, has positive effects in cultured or animal models for Parkinson's disease, Huntington's disease, and so on. However, the potential therapeutic value of GT in treating epilepsy has not yet been reported. Methods: Effects of GT on epileptic seizure (seizure) in kainic acid [KA, 55mg/kg, intraperitoneal (i.p.)]-induced model of mice, excitotoxic (hippocampal) cell death in KA [0.2 ㎍, intracerebroventricular (i.c.v.)]-induced model of mice, and levels of proinflammatory mediators in lipopolysaccharide (LPS)-induced BV2 cells were investigated. Results: An i.p. injection of KA into mice produced typical seizure. However, it was significantly alleviated by oral administration of GT in a dose-dependent manner. An i.c.v. injection of KA produced typical hippocampal cell death, whereas it was significantly ameliorated by administration of GT, which was related to reduced levels of neuroglial (microglia and astrocyte) activation and proinflammatory cytokines/enzymes expression as well as increased level of the Nrf2-antioxidant response via the upregulation of LPAR 1/3 in the hippocampus. However, these positive effects of GT were neutralized by an i.p. injection of Ki16425, an antagonist of LPA1-3. GT also reduced protein expression level of inducible nitric-oxide synthase, a representative proinflammatory enzyme, in LPS-induced BV2 cells. Treatment with conditioned medium clearly reduced cultured HT-22 cell death. Conclusion: Taken together, these results suggest that GT may suppress KA-induced seizures and excitotoxic events in the hippocampus through its anti-inflammatory and antioxidant activities by activating LPA signaling. Thus, GT has a therapeutic potential to treat epilepsy.

Neuroprotective Effect of the n-Hexane Extracts of Laurus nobilis L. in Models of Parkinson's Disease

  • Ham, Ah-Rom;Shin, Jong-Heon;Oh, Ki-Bong;Lee, Sung-Jin;Nam, Kung-Woo;Koo, Uk;Kim, Kyeong-Ho;Mar, Woong-Chon
    • Biomolecules & Therapeutics
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    • v.19 no.1
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    • pp.118-125
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    • 2011
  • Free radical scavenging and antioxidants have attracted attention as a way to prevent the progression of Parkinson's disease (PD). This study was carried out to investigate the effects of n-hexane fraction from Laurus nobilis L. (Lauraceae) leaves (HFL) on dopamine (DA)-induced intracellular reactive oxygen species (ROS) production and apoptosis in human neuroblastoma SH-SY5Y cells. Compared with apomorphine (APO, $IC_{50}=18.1\;{\mu}M$) as a positive control, the HFL $IC_{50}$ value for DA-induced apoptosis was $3.0\;{\mu}g/ml$, and two major compounds from HFL, costunolide and dehydrocostus lactone, were $7.3\;{\mu}M$ and $3.6\;{\mu}M$, respectively. HFL and these major compounds significantly inhibited ROS generation in DA-induced SH-SY5Y cells. A rodent 6-hydroxydopamine (6-OHDA) model of PD was employed to investigate the potential neuroprotective effects of HFL in vivo. 6-OHDA was injected into the substantia nigra of young adult rats and an immunohistochemical analysis was conducted to quantitate the tyrosine hydroxylase (TH)-positive neurons. HFL significantly inhibited 6-OHDA-induced TH-positive cell loss in the substantia nigra and also reduced DA induced $\alpha$-synuclein (SYN) formation in SH-SY5Y cells. These results indicate that HFL may have neuroprotective effects against DA-induced in vitro and in vivo models of PD.

Ameliorative Effects of Cirsium jaonicum, Artemisia annua and Curcuma longa on Non-alcoholic Fatty Liver Disease (엉겅퀴, 울금, 개똥쑥 복합 추출물의 지방간 개선효과)

  • Shin, Jae Young;Kang, Hyun Ju;Cho, Byoung Ok;Park, Ji Hyeon;Che, Denis Nchang;Hao, Suping;Wang, Feng;Sim, Jae Suk;Sim, Dong Jun;Jang, Seon Il
    • Korean Journal of Pharmacognosy
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    • v.51 no.3
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    • pp.178-185
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    • 2020
  • In this study, the effect of complex hot water extracts of Cirsium jaonicum, Artemisia annua and Curcuma longa (CAC) on the improvement of non-alcoholic fatty liver disease (NAFLD) was investigated. CAC inhibited fatty acid synthesis and lipid accumulation in HepG2 cells cultured with free fatty acid (FFA). In the NAFLD animal model, CAC extract suppressed the increase in body weight, liver, and epididymis fat weight, and suppressed the increase in hepatocyte fat and blood triglyceride. In addition, by blocking the Nrf2/HO-1 signaling pathway, cells were protected from oxidative stress in hepatocytes. Moreover, CAC inhibited the expression of COX-2, iNOS, TNF-α and IL-17 in hepatocytes. These results suggest the possibility that CAC extract can be applied in the field of health functional foods and pharmaceuticals for improvement and prevention of NAFLD.

Amyloid Precursor Protein Binding Protein-1 Is Up-regulated in Brains of Tg2576 Mice

  • Yang, Hyun-Jung;Joo, Yu-Young;Hong, Bo-Hyun;Ha, Sung-Ji;Woo, Ran-Sook;Lee, Sang-Hyung;Suh, Yoo-Hun;Kim, Hye-Sun
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.4
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    • pp.229-233
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    • 2010
  • Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of amyloid precursor protein and serves as a bipartite activation enzyme for the ubiquitin-like protein, NEDD8. Previously, it has been reported that APP-BP1 rescues the cell cycle S-M checkpoint defect in Ts41 hamster cells, that this rescue is dependent on the interaction of APP-BP1 with hUba3. The exogenous expression of APP-BP1 in neurons has been reported to cause DNA synthesis and apoptosis via a signaling pathway that is dependent on APP-BP1 binding to APP. These results suggest that APP-BP1 overexpression contributes to neurodegeneration. In the present study, we explored whether APP-BP1 expression was altered in the brains of Tg2576 mice, which is an animal model of Alzheimer's disease. APP-BP1 was found to be up-regulated in the hippocampus and cortex of 12 month-old Tg2576 mice compared to age-matched wild-type mice. In addition, APP-BP1 knockdown by siRNA treatment reduced cullin-1 neddylation in fetal neural stem cells, suggesting that APP-BP1 plays a role in cell cycle progression in the cells. Collectively, these results suggest that increased expression of APP-BP1, which has a role in cell cycle progression in neuronal cells, contributes to the pathogenesis of Alzheimer's disease.