• Fisheries and Aquatic Sciences
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• 제27권2호
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• pp.122-135
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• 2024

Obesity is a disease involving mechanisms of fat accumulation, low-grade inflammatory cytokine release, and mitochondrial dysfunction. The aim of the current study was to investigate the effects of abalone intestine extract on fat metabolism in 3T3-L1 adipocytes and high fat diet-induced zebrafish larvae. The total phenol content was highest in subcritical water extract at 210℃ (SW210) among hot water, ethanol, and subcritical water extracts of abalone intestine. In addition, SW210 of male abalone intestine (MASW210) most effectively controlled the lipid accumulation and expression of adipogenic or lipogenic regulators (PPAR-γ, C/EBPα, SREBP-1c, and FAS) in 3T3-L1 adipocytes. Likewise, in zebrafish larvae fed high fat, MASW210 significantly suppressed body weight, glucose levels, and lipid accumulation. The mRNA expression related to adipogenesis (PPAR-γ and C/EBPα), lipogenesis (SREBP-1c and FAS), inflammatory cytokines (TNF-α and IL-6), energy m/;.etabolism (AMPK, lepr, SIRT1, and adiponectin), and mitochondrial biogenesis (PGC-1α and CPT-1) were significantly regulated by treatment with MASW210. These results suggest that abalone intestine extract such as MASW210, are useful biomaterials for improving obesity and metabolic diseases.

• 생명과학회지
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• 제28권2호
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• pp.170-175
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• 2018

파킨슨병은 두번째로 많이 발병하는 퇴행성 신경질환이며 약 5-10%는 유전된다. Leucine-rich repeat kinase 2(LRRK2)는 그 돌연변이의 일부가 파킨슨병을 일으키는 유전자이다. LRRK2에는 인산화효소와 GTPase 기능이 있는 도메인과 함께 단백질 상호작용에 관여하는 Leucine-rich repeat (LRR), WD40 도메인이 존재하여, LRRK2와 상호작용하는 단백질이 파킨슨병 발병에 중요한 역할을 함을 암시한다. 우리는 이러한 LRRK2와 상호작용하는 단백질을 규명하여 그 단백질의 세포내 기능을 통해 역으로 LRRK2의 기능을 밝히고자 하였다. NIH3T3 세포 용해물을 LRRK2 항체와 IgG로 각각 면역침강하여 LRRK2 항체 침강반응에서만 특이적으로 나타나는 단백질 밴드를 질량 분석한 결과, methionyl-tRNA synthetase (MRS)로 나타났다. LRRK2와 MRS의 상호작용은 면역침강반응과 GST-pull down assay를 통해 확인됐다. 병을 유발하는, LRRK2의 돌연변이인 G2019S가 인산화효소 활성을 증가시키므로 LRRK2가 MRS를 인산화하는 지를 조사한 결과, LRRK2재조합단백질은 MRS 단백질을 인산화 하지 않았다. 또한 이들 두 단백질의 각각의 양 증가가 상대 단백질의 양 증가, 즉 안정성에 영향을 미치는 지를 조사하였으나 안정성의 변화를 관찰하지 못하였다. 결론적으로, MRS는 LRRK2와 상호작용을 하지만 LRRK2 인산화효소의 기질은 아니다.

• Journal of Periodontal and Implant Science
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• 제27권4호
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• pp.669-684
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• 1997

Polypeptide growth factors belong to a class of potent biologic mediators which regulate cell differentiation, proliferation, migration and metabolism. IGF-I is polypeptides secreted by skeletal cells and is considered as regulators of bone formation. The purpose of this study is to evaluate the effects of IGF-I on bone nodule formation and alkaline phosphatase activity of MC3T3-E1 cells. MC3T3-E1 cells were seeded at $1{\times}10^4$ cells/well, $1{\times}10^5$ cells/well in alpha-modified Eagle medium containing 10% fetal bovine serum, 10 mM ${\beta}-glycerophosphate$ and $5O{\mu}g/ml$ of ascorbic acid. Before 48 hours of indicated time, medium were changed with serum free medium. After 24 hours, 0.1, 1, 10 ng/ml IGF-I were added to the cells and cultured for 3, 7, 14, 21, 28 days. And histochemical analysis was done and ALP activity was measured and was expressed as nmol/min/mg of protein. The bone nodule formation in MC3T3-E1 cells of IGF-I was seen at 21, 28 days, but there were no difference between control group and experimental groups. The ALP activity decreased when it is compare to control 2 group except for 1 ng/ml, 10 ng/ml IGF-I of 21-day-groups and 1 ng/ml IGF-I of 28-day-groups. Dose response effects of IGF-I of ALP activity in MC3T3-E1 cells were seen the highest ALP activity at 1ng/ml until 21days and the highest ALP activity at 10 ng/ml of 28 daygroups. The peak times were seen at 7-day group, 14-day group on control group and experimental group respectively, and 1 ng/ml group was the highest ALP activity, From the above results, IGF-I was not seen notable effect on bone nodule formation and decreased ALP activity of MC3T3-E1 cells but the use of IGF-I to mediate biological stimulation of MC3T3-E1 cells shows promise for future therapeutic application.

• IMMUNE NETWORK
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• 제11권5호
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• pp.227-244
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• 2011

MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their target messenger RNAs (mRNAs). Recent studies have clearly demonstrated that miRNAs play critical roles in several biologic processes, including cell cycle, differentiation, cell development, cell growth, and apoptosis and that miRNAs are highly expressed in regulatory T (Treg) cells and a wide range of miRNAs are involved in the regulation of immunity and in the prevention of autoimmunity. It has been increasingly reported that miRNAs are associated with various human diseases like autoimmune disease, skin disease, neurological disease and psychiatric disease. Recently, the identification of miRNAs in skin has added a new dimension in the regulatory network and attracted significant interest in this novel layer of gene regulation. Although miRNA research in the field of dermatology is still relatively new, miRNAs have been the subject of much dermatological interest in skin morphogenesis and in regulating angiogenesis. In addition, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributions to neurodegenerative disorder. Moreover, there is now compelling evidence that dysregulation of miRNA networks is implicated in the development and onset of human neruodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Tourette's syndrome, Down syndrome, depression and schizophrenia. In this review, I briefly summarize the current studies about the roles of miRNAs in various autoimmune diseases, skin diseases, psychoneurological disorders and mental stress.

• International Journal of Oral Biology
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• 제37권1호
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• pp.31-36
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• 2012

Dlx3 and Dlx5 are homeobox domain proteins and are well-known regulators of osteoblastic differentiation. Since possible reciprocal relationships between osteogenic and adipogenic differentiation in mesenchymal stem cells exist, we examined the regulatory role of Dlx3 and Dlx5 on adipogenic differentiation using human dental pulp stem cells. Over-expression of Dlx3 and Dlx5 stimulated osteogenic differentiation but inhibited adipogenic differentiation of human dental pulp stem cells. Dlx3 and Dlx5 suppressed the expression of adipogenic marker genes such as $C/EBP{\alpha}$, $PPAR{\gamma}$, aP2 and lipoprotein lipase. Adipogenic stimuli suppressed the mRNA levels of Dlx3 and Dlx5, whereas osteogenic stimuli enhanced the expression of Dlx3 and Dlx5 in 3T3-L1 preadipocytes. These results suggest that Dlx3 and Dlx5 exert a stimulatory effect on osteogenic differentiation of stem cells through the inhibition of adipogenic differentiation as well as direct stimulation.

• Journal of Ginseng Research
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• 제29권2호
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• pp.71-79
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• 2005

In vitro studies using detached inflorescences with peduncles were conducted to investigate flower abscission agents in North American ginseng (Panax quinquefolius L.). Of the nine compounds studied only three, ammonium thiosulphate (ATS), abscisic acid (ABA) and ethephon induced abscission. Anilazine, benzyladenine, carbaryl, gibberellic acid, napthaleneacetic acid and thidiazuron did not induce abscission. ATS dip treatments did not induce abscission but the spray treatments induced $60.5\%$ abscission at $1500\;mg{\cdot}L^{-1}$ and $33.1\%$ at $3000\;mg{\cdot}L^{-1}$. Severe chlorophyll loss occurred on all inflorescences treated with ATS. Both ABA dip treatments and a $250\;{\mu}mol{\cdot}L^{-1}$ spray treatment caused abscission $(40\%)$ without adverse effects, and timing of ABA application was important. Because ABA was only significant in the dip treatments, ABA may not be a practical option for field use on ginseng. Ethephon sprays induced more abscission as the season progressed and as the concentration increased. As the dip concentrations of ethephon increased, the abscission rate decreased and the health of the inflorescences declined. The $1500\;mg{\cdot}L^{-1}$ spray of ethephon gave consistent abscission results over the glowing season with little phytotoxicity. Treatment with the competitive ethylene inhibitor 1-methylcy-clopropene (1-MCP) suggested that flower abscission was due to the liberation of ethylene from the breakdown of ethephon.

• 한국약용작물학회지
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• 제9권1호
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• pp.15-20
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• 2001

하늘타리 (T. kirilowii)의 기내 (in vitro) 대량증식을 위하여 줄기절편을 2 mg/L BA가 첨가된 MS 배지에 치상하였을 때 정단부위가 포함된 줄기절편의 기저부로부터 다수의 부정아가 형성되었다. 부정아는 정상적인 신초로 분화하였으며, 이와같이 형성 된 신초는 0.5 mg/L BA가 첨가된 MS 배지로 옮겼을 때 4주 후 시료당 $17.3{\pm}0.2$개의 신초로 재분화하였다. 신초의 증식에 있어서 배지내 탄소원으로는 3% sucrose가 적절하였으며, 고형물질에 의한 영향은 확인할 수 없었다. 한편 신초의 발근은 무기염 의 농도가 절반으로 줄어 든 1/2MS 배지 (2% sucrose, 0.3% phytagel, pH 5.7)에서 신초당 $4.3{\pm}0.02$개로 96%이상 형성 되었다.

• Molecules and Cells
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• 제37권9호
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• pp.685-690
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• 2014

Osteoclasts are large polykaryons that have the unique capacity to degrade bone and are generated by the differentiation of myeloid lineage progenitors. To identify the genes involved in osteoclast development, we performed microarray analysis, and we found that carboxypeptidase E (CPE), a prohormone processing enzyme, was highly upregulated in osteoclasts compared with their precursors, bone marrow-derived macrophages (BMMs). Here, we demonstrate a novel role for CPE in receptor activator of NF-${\kappa}B$ ligand (RANKL)-induced osteoclast differentiation. The overexpression of CPE in BMMs increases the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear osteoclasts and the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1), which are key regulators in osteoclastogenesis. Furthermore, employing CPE knockout mice, we show that CPE deficiency attenuates osteoclast formation. Together, our data suggest that CPE might be an important modulator of RANKL-induced osteoclast differentiation.

• Asian Journal of Business Environment
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• 제11권4호
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• pp.5-16
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• 2021

Purpose: This study aims to investigate the impact of auditor-client traffic convenience on accrual -based and real earnings management of the client firms. Research design, data and methodology: Using a sample of firms listed in Shanghai and Shenzhen Stock Exchanges over the period of 2007 to 2018, this paper empirically investigates the association between auditor-client traffic convenience and earnings management. We use three measures of auditor-client traffic convenience: railway traffic convenience, expressway traffic convenience, and air traffic convenience. The accrual-based earnings management is measured by abnormal accruals estimated by industry and year using the Modified Jones Model. Results: Findings indicate that traffic convenience is conducive to detecting and restraining positive accrual earnings management and real earnings management. After changing the measurement of independent variable and dependent variable, including potential omitted variables, the results are statistically unchanged. Further, the research shows that traffic convenience can not only improve audit quality, but also lead to higher fee premiums. Auditors didn't share with clients the cost reduction benefits caused by traffic convenience. Conclusions: Traffic convenience provides auditors with easy access to the client firms, alleviating the information asymmetry and improving corporate earnings quality. The findings have implications for regulators, audit practitioners and stakeholders.

• Nutrition Research and Practice
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• 제8권6호
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• pp.655-661
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• 2014

BACKGROUND/OBJECTIVES: The purpose of this study was to examine the effects and associated mechanisms of arctiin, a lignan compound found in burdock, on adipogenesis in 3T3-L1 cells. Also, the effects of arctiin supplementation in obese mice fed a high-fat diet on adiposity were examined. MATERIALS/METHODS: 3T3-L1 cells were treated with arctiin (12.5 to $100{\mu}M$) during differentiation for 8 days. The accumulation of lipid droplets was determined by Oil Red O staining and intracellular triglyceride contents. The expressions of genes related to adipogenesis were measured by real-time RT-PCR and Western blot analyses. For in vivo study, C57BL/6J mice were first fed either a control diet (CON) or high-fat diet (HF) to induce obesity, and then fed CON, HF, or HF with 500 mg/kg BW arctiin (HF + AC) for four weeks. RESULTS: Arctiin treatment to 3T3-L1 pre-adipocytes markedly decreased adipogenesis in a dose-dependent manner. The arctiin treatment significantly decreased the protein levels of the key adipogenic regulators $PPAR{\gamma}$ and $C/EBP{\alpha}$, and also significantly inhibited the expression of SREBP-1c, fatty acid synthase, fatty acid-binding protein and lipoprotein lipase. Also, arctiin greatly increased the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target phosphorylated-acetyl CoA carboxylase. Furthermore, administration of arctiin significantly decreased the body weight in obese mice fed with the high-fat diet. The epididymal, perirenal or total visceral adipose tissue weights of mice were all significantly lower in the HF + AC than in the HF. Arctiin administration also decreased the sizes of lipid droplets in the epididymal adipose tissue. CONCLUSIONS: Arctiin inhibited adipogenesis in 3T3-L1 adipocytes through the inhibition of $PPAR{\gamma}$ and $C/EBP{\alpha}$ and the activation of AMPK signaling pathways. These findings suggest that arctiin has a potential benefit in preventing obesity.