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강보빈,김채영,황지수,선소정,양현원,서형주,최현선 한국식품과학회 2019 Food Science and Biotechnology Vol.28 No.6
This study was aimed to investigate the effect ofred ginseng extract (RGE) on monocyte to macrophagedifferentiation and inflammatory signalings in THP-1human monocytes. In HPLC analysis, RGE containedsaponin level of 516 lg/mg (extract) with 14 ginsenosides. RGE effectively suppressed the monocyte-to-macrophagedifferentiation induced by phorbol 12-myristate 13-acetated(PMA) by inhibiting the THP-1 cell adhesion. Thisresult is evidenced by the down-regulation of cluster ofdifferentiation molecule b (CD11b) and CD36. RGE significantlyreduced translocation of nuclear factor kappalight-chain-enhancer of activated B cells (NF-jB) (78%),while cytosolic NF-jB was increased (53%), comparedwith LPS group. In addition, RGE significantly increasedthe protein abundance of nuclear factor (erythroid-derived2)-like 2 (Nrf2) and its target protein, hemoxygenase-1(HO-1), but, Kelch-like ECH-associated protein 1(KEAP1), a negative regulator of Nrf2, was greatlydecreased by RGE. Furthermore, RGE effectivelymediated the regulation of Nrf2 level in nucleus andcytoplasm of THP-1.
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홍삼 비사포닌 분획의 단핵세포 분화와 염증반응에 대한 억제효과
강보빈(Bobin Kang),김채영(Chae Young Kim),황지수(Jisu Hwang),최현선(Hyeon-Son Choi) 한국식품과학회 2019 한국식품과학회지 Vol.51 No.1
본 연구에서는 홍삼 비사포닌 분획(NSF)의 항 염증 효과를 마우스 대식세포와 인간유래 단핵세포에서 확인하였다. NSF는 마우스 대식세포에서 LPS로 유도된 NO, iNOS 그리고 COX-2의 양 뿐만 아니라 IL-6, TNF-α, MCP-1과 같은 염증성 싸이토카인의 생성량을 유의적으로 감소시켰다. 인간 유래 단핵세포에서는 PMA에 의해 유도되는 대식세포로의 분화를 효과적으로 억제하면서 분화인자인 CD11β와 CD36의 발현을 유의적으로 감소시켰다. 마우스 대식세포에서와 마찬가지로 염증성 싸이토카인들의 생성량 또한 감소하였는데, 이러한 NSF의 항 염증 효과는 두 전사인자의 조절작용에 의한 것으로 사료된다. 즉 NSF는 NF-κB의 핵으로 이동을 감소시킴으로써 전사활성을 억제하여 염증성 싸이토카인들의 발현을 저해하고 이와 반대로 Nrf2의 발현과 핵으로의 이동을 증가시켜 항산화 효소이면서 항 염증 작용을 나타내는 HO-1의 발현을 촉진하는 것으로 관찰되었다. 따라서 NSF는 NF-κB와 Nrf2의 두 가지 신호전달체계를 조절함으로써 항 염증 작용을 나타냈으며 이를 홍삼 NSF의 항 염증 기작으로 보고하는 바이다. The aim of this study was to investigate the effects of red ginseng-derived non-saponin fraction (NSF) on inflammatory responses and monocyte-to-macrophage differentiation in RAW264.7 and THP-1. NSF effectively inhibited inflammatory responses by downregulating nitric oxide (NO) production and protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). NSF (2000 μg/mL) decreased the levels of NO, iNOS, and COX-2 by 33, 83, and 64%, respectively. NSF inhibited the differentiation of monocyte-to-macrophage by decreasing cell adherence along with downregulation of the cluster of differentiation molecule 11β (CD11β) and CD36. In addition, pro-inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin 6, and monocyte chemoattractant protein 1 (MCP-1), were significantly reduced with NSF treatment. The NSF-mediated inhibition of inflammatory responses was due to the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). NSF effectively suppressed the translocation of NF-κB into the nucleus, while nuclear Nrf2 and its target protein, heme oxygenase-1, levels were significantly increased.
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김채영,강보빈,홍정일,최현선 한국식품과학회 2020 Food Science and Biotechnology Vol.29 No.3
The effects of parthenolide (PL), a sesquiterpene lactone obtained from feverfew plant, on lipid accumulation and signaling pathway in adipocytes were investigated. PL significantly inhibited lipid accumulation and adipogenic factors during adipogenesis. In particular, PL exerted its inhibitory effects in early adipogenic stage by regulating the early adipogenic factors. In addition, PL regulated the expression of adipokines; leptin, retinol binding protein, and resistin mRNAs were downregulated, whereas adiponectin gene expression was increased. Furthermore, PL significantly reduced intracellular reactive oxygen species (ROS) production during adipogenesis. This PL-mediated regulation of ROS production was associated with the regulation of nuclear factor erythroid 2-related factor (Nrf2)-kelch-like ECH-associated protein 1 (Keap1) pathway. PL effectively increased the abundance of Nrf2 and its target proteins, heme oxygenase-1 (HO-1) and NADPH dehydrogenase 1 (NQO1), by promoting the nuclear translocation of Nrf2, indicating that PL-mediated anti-adipogenic effects are associated with the Nrf2/Keap1 pathway.
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홍삼 사포닌 분획의 Nrf2 Keap1 신호전달체계 조절을 통한 지방축적 및 활성산소종 억제효과
김채영,강보빈,황지수,최현선 한국식품과학회 2018 한국식품과학회지 Vol.50 No.6
This study aimed to investigate the effects of red ginseng-derived saponin fraction (SF) on lipid accumulation, reactive oxygen species (ROS) production, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling during adipocyte differentiation. SF effectively inhibited lipid accumulation, with the downregulation of adipogenic factors such as peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancerbinding protein alpha (C/EBPα). A high dose of SF decreased the protein levels of PPARγ and C/EBPα by over 90% compared to the control. SF-mediated downregulation of adipogenic factors was due to the regulation of early adipogenic factors including C/EBPβ and Krüppel-like Factor 2 (KLF2). In addition, SF (200 μg/mg) decreased intracellular ROS generation by 40% during adipocyte differentiation. However, the SF significantly upregulated Nrf2 and its target proteins, hemoxygenase-1 (HO-1) and NADPH dehydrogenase quinone 1 (NQO1). Furthermore, SF (200 μg/mg) promoted the nuclear translocation of Nrf2. The SF-mediated reduction of lipid accumulation was associated with the regulation of the Nrf2/Keap1 pathway.
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서형주,강보빈,김채영,최현선 한국식품저장유통학회 2017 한국식품저장유통학회지 Vol.24 No.4
The purpose of current study is to investigate the beneficial effect of enzyme (Alcalase) hydrolysates of silk protein in rat. Alcalase-treated silk protein hydrolysate (ATSH) itself did not show any cytotoxicity on the hepatic tissues and blood biochemistry, similar to the normal condition. ATSH played a protective role in tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. The values of AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are the indicators of the liver function, were effectively alleviated with the ATSH treatment in a dose dependent manner. The level of Lactate dehydrogenase (LDH) and Malondialdehyde (MDA), which were increased with t-BHP treatment, were significantly reduced by ATSH. High dose of ATSH (2 g/kg) reduced the t-BHP-induced LDH release by 48%. Antioxidant and antioxidant enzymes in liver cells were significantly increased by ATSH treatment in their level and activities. ATSH (2 g/kg) increased glutathione (GSH), an intracelluar antioxidant, by 2.5-fold compared with the t-BHP treated group. The activities of glutathione-s-transferase (GST), superoxide dismutase (SOD), and catalase were also elevated by 38%, 60%, and 45%, respectively, with ATSH (2 g/kg) treatment. The antioxidative effect of ATSH was recapitulated to the protection from t-BHP induced liver damages in hematoxylin and eosin (H&E) staining. Thus, ATSH might be used as a hepatoprotective agent.
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