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        검색결과 5

        1.
        2018.04 구독 인증기관·개인회원 무료
        Nanostructured lipid carriers (NLC) are getting attention as delivery system for nutraceuticals due to its low toxicity and higher loading efficiency of active ingredients. However, the cytotoxicity of NLC had not fully evaluated especially on neuroblastoma. In this study, cytotoxicity of NLC and curcumin-loaded NLC (C-NLC) were evaluated on SH-SY5Y neuroblastoma cells investigating cell morphology, mitochondrial activity, and reactive oxygen species (ROS) production compared to H2O2 treatment as a positive control. As a result, the metabolic activity was inhibited about 40% by 250ppm of NLC along with morphological change. C-NLC exhibited 50% inhibitory effect on mitochondrial activity at 500ppm, which was lower than NLC itself. Moreover, NLCs significantly induced ROS production which was recognized as one of the indicators of cytotoxicity generated by NLCs. In conclusion, lower cytotoxic effect was observed with NLC on SH-SY5Y neuroblastoma based on ROS production and these investigation could be used for further application of NLC in food industry.
        2.
        2017.05 서비스 종료(열람 제한)
        Background : We have previously reported that Oligonol, a low-molecular polyphenol derived from lychee fruit, has protective effect on the liver and kidney of diabetic animal model. In this study, we examined whether Oligonol has any beneficial effects on pancreas of diabetic rats. Methods and Results : Oligonol was orally administered at a dose of 10 and 20 mg/kg body weight for 10 days to STZ-induced diabetic rats, and the effects were compared with those of vehicle-treated diabetic control and non-diabetic control rats. The administration of Oligonol reduced hyperglycemia in diabetic rats through an improvement of serum and pancreatic insulin levels. The increased reactive oxygen species levels in pancreas of diabetic control rats was attenuated by the Oligonol administration through inhibiting the expression of NADPH oxidase-related proteins. The enhanced expression of pro-apoptotic proteins in pancreas of diabetic control rats was significantly reduced by Oligonol administration through down-regulation of phosphor-c-Jun N-terminal kinases protein in pancreas. Furthermore, the expressions of cell proliferation-related protein were also augmented in Oligonol treated-diabetic rats. However, Oligonol treatment led to improved histological changes in the pancreas. Conclusion : These pancreatoprotective effects of Oligonol were achieved through attenuation of oxidative stress and its sensitive protein expression associated with apoptosis and cell proliferation in diabetic rats.
        3.
        2015.10 KCI 등재 SCOPUS 서비스 종료(열람 제한)
        본 연구에서는 연화 열수 및 에탄올 추출물의 3T3-L1 지방세포 분화 및 ROS생성 저감효과를 구명하기 위하여 3T3-L1 전지방세포 분화과정 중 연화 열수 및 에탄올 추출 물에 의한 지방축적과 ROS 생성을 관찰하였다. 연화 열수 및 에탄올 추출물은 XTT assay에서 100, 200 및 400 μg/mL 농도에서 세포 독성을 보이지 않았다. 지방세포 분화 중 세포 내 지방축적 및 ROS 생성량을 비교한 결과, 연화 열수 및 에탄올 추출물을 처리한 지방세포의 경우 지방축적량과 ROS 생성량 모두 유의적으로 억제되는 것으로 나타났다. 특히 연화 열수 및 에탄올 추출물을 처리함으로써 지방세포 분화와 관련된 전사인자인 PPARγ, C/EBPα 및 aP mRNA의 발현을 유의적으로 감소시켰으며, ROS의 생성과 관련이 있는 주요 유전자인 NOX4 및 catalase의 유전자발현 또한 유의적으로 감소하였다. 이 결과를 통해 연화 열수 및 에탄 올 추출물이 3T3-L1 지방세포 내 중성지방의 축적 억제 효과와 더불어 ROS 생성 억제에 효과적으로 작용함을 확인 하였다. 따라서 연화 열수 및 에탄올 추출물은 비만과 같은 대사증후군 관련 질환의 개선을 위한 천연물 기능성 소재로 의 활용이 기대된다.
        4.
        2012.06 KCI 등재 SCOPUS 서비스 종료(열람 제한)
        Obesity, a strong risk factor for the development of chronic diseases, is characterized by an increase in the number and size of adipocytes differentiated from precursor cells, preadipocytes. Recent research suggests that increased reactive oxygen species (ROS) production in 3T3-L1 adipocyte facilitates adipocyte differentiation and fat accumulation. This study was to investigate whether reduced ROS production by Sargassum micracanthum extract (SME) could protect the development of obesity through inhibition of adipogenesis. 3T3-L1 preadipocytes were treated SME for up to 8 days following standard induction of differentiation. The extent of differentiation reflected by amount of lipid accumulation and ROS production was determined by Oil red O staining and nitroblue tetrazolium (NBT) assay. Treatment of SME significantly inhibited ROS production and adipocyte differentiation that is depend on down regulation of NADPH oxidase 4 (NOX4), a major ROS generator, and peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), a key adipogenic transcription factor. These results indicate that SME can inhibit adipogenesis through a reduced ROS level that involves down-regulation of NOX4 expression or via modulation of adipogenic transcription factor.
        5.
        2012.06 KCI 등재 SCOPUS 서비스 종료(열람 제한)
        Recently, NADPH oxidase 4 (NOX4)-mediated generation of intracellular reactive oxygen species (ROS) was proposed to accelerate adipogenesis of 3T3-L1 cell. We have previously shown that Cheonnyuncho (Opuntia humifusa) extract significantly inhibited adipocyte differentiation via downregulation of PPARγ (peroxisome proliferator-activated receptor gamma) gene expression. In this study, we focused on the molecular mechanism(s) of NOX4, G6PDH (glucose-6-phosphate dehydrogenase) and antioxidant enzymes in anti-oxidative activities of 3T3-L1 adipocytes. Our results indicate that Cheonnyuncho extracts markedly inhibits ROS production during adipogenesis in 3T3-L1 cells. Cheonnyuncho extracts suppressed the mRNA expression of the pro-oxidant enzyme such as NOX4 and theNADPH-producing G6PDH enzyme. In addition, treatment with Cheonnyuncho extract was found to upregulate mRNA levels of antioxidant enzymes such as Mn-SOD (manganese-superoxide dismutase), Cu/Zn-SOD (copper/zinc-SOD), glutathione peroxidase (GPx), glutathion reductase (GR), and catalase, all of which are important for endogenous antioxidant responses. These data suggest that Cheonnyuncho extract may be effective in preventing the rise of oxidative stress during adipocyte differentiation through mechanism(s) that involves direct down regulation of NOX4 and G6PDH gene expression or via upregulation of endogenous antioxidant responses.