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소부혈(少府穴) 자침(刺鍼)이 Kainic Acid로 유도(誘導)된 간질(癎疾) 동물(動物)모델의 해마(海馬) 치상회(齒狀回)에 미치는 영향(影響)
김승태 ( Seung Tae Kim ),정주호 ( Joo Ho Chung ),정우병 ( Wu Byung Jeong ),김장현 ( Jang Hyun Kim ),강민정 ( Min Jung Kang ),홍미숙 ( Mee Sook Hong ),박해정 ( Hae Jeong Park ),김연정 ( Yeon Jung Kim ),박히준 ( Hi Joon Park ),이혜 대한경락경혈학회 2007 Korean Journal of Acupuncture Vol.24 No.4
Objectives: Epilepsy is one of the most common serious brain disorders that affect people of all ages, and it is characterized by recurrent unprovoked seizures. We examined whether acupuncture can reduce both the incidence of seizures and hippocampal cell death in dentate gyrus (DG) using a mouse model of kainic acid (KA)-induced epilepsy. Methods: ICR mice (20~25g) were given acupuncture once a day at acupoint HT8 (sobu) bilaterally during 2 days before KA injection. After an intracerebroventricular injection of 0.1μg of KA, acupuncture treatment was subsequently administered once more (total 3 times), and the degree of seizure was observed for 20 min. Three hours after injection, we confirmed the neural cell death using cresyl violet staining and silver impregnation staining, and determined the expressions of c-Fos and glutamate decarboxylase (GAD)-67 using immunohistochemistry techniques in the DG. Results: KA induced epileptic seizure, neural cell death, increased c-Fos expression and decreased GAD-67 expression in the DG. Acupuncture treatment at HT8 reduced the severity of the epileptic seizure and inhibited neural cell death from KA. In addition, acupuncture normalized the expressions of c-Fos and GAD-67 in the same areas. Conclusions: These results demonstrated that acupuncture treatment at HT8 may reduce the KA-induced epileptic seizure and neural cell death in the DG possibly by normalizing c-Fos expressions and the gamma-aminobutyric acid neurons.
Wu, Hong Min,Lee, Chan Gyu,Hwang, Se Jin,Kim, Sang Geon Wiley (Blackwell Publishing) 2014 British journal of pharmacology Vol.171 No.11
<P>Methylene blue (MB) has recently been considered for new therapeutic applications. In this study, we investigated whether MB has antioxidant and mitochondria-protecting effects and can prevent the development of toxicant-induced hepatitis. In addition, we explored the underlying basis of its effects.</P>
Hong Yan,Min Zhao,Shan Huang,Ping Chen,Wen-yong Wu,Jin Huang,Zheng-sheng Wu,Qiang Wu 한국유방암학회 2016 Journal of breast cancer Vol.19 No.1
Purpose: Prolactin (PRL) plays a critical role in breast cancer progression by activating its cognate receptor and promotes the growth and differentiation of breast cancer cells. Studies have shown that B-cell lymphoma 6 (BCL6) is the target gene of microRNA- 339-5p (miR-339-5p) and that BCL6 expression contributes to breast cancer progression. Herein, we identified PRL as a potent suppressor of BCL6 expression in human breast cancer cells. Methods: Western blotting and quantitative reverse transcription-polymerase chain reaction were used to investigate molecular mechanisms underlying miR-339-5p expression and BCL6 manipulation in MCF-7, T47D, and SKBR3 breast cancer cells. Phenotypic changes in these breast cancer cell lines were assessed by performing cell viability (MTT), colony formation, migration, and invasion assays. Results: PRL suppressed BCL6 protein and mRNA expression and upregulated miR-339-5p expression in MCF-7 and T47D breast cancer cells. Selective downregulation of miR-339-5p expression significantly reversed PRL-induced suppression of BCL6 mRNA and protein expression. Exogenous PRL stimulation significantly decreased the proliferation, colony formation, migration, and invasion of breast cancer cells, and suppression of miR-339-5p expression reversed these processes in vitro. Conclusion: These results indicated that PRL inhibited BCL6 expression and regulated breast cancer progression through a miR-339-5p-dependent pathway.
Hong-Lin Xu,Guang-Hong Chen,Yu-Ting Wu,Ling-Peng Xie,Zhang-Bin Tan,Bin Liu,Hui-Jie Fan,Hong-Mei Chen,Gui-Qiong Huang,Min Liu,Ying-Chun Zhou 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1
Background: Panax ginseng Meyer (P. ginseng), a herb distributed in Korea, China and Japan, exerts benefits on diverse inflammatory conditions. However, the underlying mechanism and active ingredients remains largely unclear. Herein, we aimed to explore the active ingredients of P. ginseng against inflammation and elucidate underlying mechanisms. Methods: Inflammation model was constructed by lipopolysaccharide (LPS) in C57BL/6 mice and RAW264.7 macrophages. Molecular docking, molecular dynamics, surface plasmon resonance imaging (SPRi) and immunofluorescence were utilized to predict active component. Results: P. ginseng significantly inhibited LPS-induced lung injury and the expression of proinflammatory factors, including TNF-a, IL-6 and IL-1b. Additionally, P. ginseng blocked fluorescence-labeled LPS (LPS488) binding to the membranes of RAW264.7 macrophages, the phosphorylation of nuclear factor-kB (NF-kB) and mitogen-activated protein kinases (MAPKs). Furthermore, molecular docking demonstrated that ginsenoside Ro (GRo) docked into the LPS binding site of toll like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) complex. Molecular dynamic simulations showed that the MD2-GRo binding conformation was stable. SPRi demonstrated an excellent interaction between TLR4/MD2 complex and GRo (KD value of 1.16 × 10<SUP>-9</SUP> M). GRo significantly inhibited LPS488 binding to cell membranes. Further studies showed that GRo markedly suppressed LPS-triggered lung injury, the transcription and secretion levels of TNF-α, IL-6 and IL-1β. Moreover, the phosphorylation of NF-kB and MAPKs as well as the p65 subunit nuclear translocation were inhibited by GRo dose-dependently. Conclusion: Our results suggest that GRo exerts anti-inflammation actions by direct inhibition of TLR4 signaling pathway.
Wu, Hong Min,Yang, Yoon Mee,Kim, Sang Geon American Society for Pharmacology and Experimental 2011 Molecular pharmacology Vol.80 No.5
<P>Liver X receptor-α (LXRα) and its target sterol regulatory element-binding protein-1c (SREBP-1c) play key roles in hepatic lipogenesis. Rimonabant, an inverse agonist of cannabinoid receptor type 1 (CB1), has been studied as an antiobesity drug. In view of the link between CB1 and energy metabolism, this study investigated the effect of rimonabant on LXRα-mediated lipogenesis in hepatocytes and the underlying basis. Rimonabant treatment inhibited CYP7A1-LXRα response element gene transactivation and an increase in LXRα mRNA level by the LXRα agonist N-(2,2,2-trifluoroethyl)-N-[4-[2,2,2-trifluoro-1-hydroxy-1-(trifluoromethyl)ethyl]phenyl]-benzenesulfonamide (T0901317) in HepG2 cells. Rimonabant consistently attenuated the activation of SREBP-1c and its target gene induction. The reversal by CB1 agonists on rimonabant's repression of SREBP-1c supported the role of CB1 in this effect. Rimonabant inhibited the activation of SREBP-1c presumably via Gα(i/o) inhibition, as did pertussis toxin. Adenylyl cyclase activator forskolin or 8-bromo-cAMP treatment mimicked the action of rimonabant, suggesting that Gα(i/o) inhibition causes repression of SREBP-1c by increasing the cAMP level. Knockdown or chemical inhibition of protein kinase A (PKA) prevented the inhibition of LXRα by rimonabant, supporting the fact that an increase in cAMP content and PKA activation, which catalyzes LXRα inhibitory phosphorylation, might be responsible for the antilipogenic effect. In addition, rimonabant activated liver kinase B1 (LKB1), resulting in the activation of AMP-activated protein kinase responsible for LXRα repression. Moreover, PKA inhibition prevented the activation of LKB1, supporting the fact that PKA regulates LKB1. In conclusion, rimonabant has an antilipogenic effect in hepatocytes by inhibiting LXRα-dependent SREBP-1c induction, as mediated by an increase in PKA activity and PKA-mediated LKB1 activation downstream of CB1-coupled Gα(i/o) inhibition.</P>
Shi-Min Wu,Tian-Hong Li,Hao Yun,Hong-Wu Ai,Ke-Hui Zhang 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.6
Purpose: Liver fibrosis is a major cause of morbidity and mortality and the outcome of various chronic liver diseases. Activationof hepatic stellate cells (HSCs) is the key event in liver fibrosis. Studies have confirmed that miR-140-3p plays a potential regulatoryeffect on HSC activation. However, whether miR-140-3p mediates the liver fibrosis remains unknown. Materials and Methods: Expression of miR-140-3p was detected by real-time quantitative PCR (qPCR). Cell proliferation wasmeasured by MTT, while cell apoptosis rate was determined via flow cytometry. Western blot assay was used to detect the expressionof cleaved PARP. The fibrogenic effect was evaluated by expression of α-smooth muscle actin and desmin. Functional experimentswere performed in transforming growth factor β1 (TGF-β1)-induced HSC-T6 cells with transfection of anti-miR-140-3pand/or siPTEN. Target binding between miR-140-3p and PTEN was predicted by the TargetScan database and identified usingluciferase reporter assay and RNA immunoprecipitation. Results: TGF-β1 induced the activation of HSC-T6 cells, and miR-140-3p expression varied according to HSC-T6 cell activationstatus. Knockdown of miR-140-3p reduced cell proliferation and the expressions of α-SMA and desmin, as well as increasedapoptosis, in TGF-β1-induced HSC-T6 cells, which could be blocked by PTEN silencing. Additionally, inactivation of the AKT/mTOR signaling pathway stimulated by miR-140-3p knockdown was abolished when silencing PTEN expression. PTEN was negativelyregulated by miR-140-3p via direct binding in HSC-T6 cells. Conclusion: miR-140-3p is an important mediator in HSC-T6 cell activation, and miR-140-3p knockdown suppresses cell proliferationand fibrogenesis in TGF-β1-induced HSC-T6 cells, indicating that miR-140-3p may be a potential novel molecular targetfor liver fibrosis.
Electrochemical preparation of Co<sub>3</sub>Pt nanowires
Min, Ji Hyun,Wu, Jun Hua,Cho, Ji Ung,Lee, Ju Hun,Ko, Young-Dong,Liu, Hong-Ling,Chung, Jin-Seok,Kim, Young Keun WILEY-VCH Verlag 2007 Physica status solidi. PSS. A, Applications and ma Vol.204 No.12
<P>Fabrication of Co-Pt nanowire arrays with fcc-Co<SUB>3</SUB>Pt phase was accomplished by DC electrodeposition in anodic aluminum oxide (AAO) nanotemplates. The microstructural and magnetic properties of the nanowires were investigated as a function of the deposition current density (Co concentration). The nanowires possess fcc-Co<SUB>3</SUB>Pt phases and are ferromagnetic. Their crystallinity and magnetic performance was enhanced after annealing. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)</P>
( Min Wu Jie Tang ),( Xuerui Zhou ),( Dan Lei ),( Chaoyi Zeng ),( Hong Ye Ting Cai ),( Qing Zhang ) 한국미생물 · 생명공학회 2022 Journal of microbiology and biotechnology Vol.32 No.2
Continued fenvalerate use has caused serious environmental pollution and requires large-scale remediation. Dibutyl phthalate (DBP) was discovered in fenvalerate metabolites degraded by Citrobacter freundii CD-9. Coculturing is an effective method for bioremediation, but few studies have analyzed the degradation pathways and potential mechanisms of cocultures. Here, a DBPdegrading strain (BDBP 071) was isolated from soil contaminated with pyrethroid pesticides (PPs) and identified as Stenotrophomonas acidaminiphila. The optimum conditions for DBP degradation were determined by response surface methodology (RSM) analysis to be 30.9 mg/l DBP concentration, pH 7.5, at a culture temperature of 37.2℃. Under the optimized conditions, approximately 88% of DBP was degraded within 48 h and five metabolites were detected. Coculturing C. freundii CD-9 and S. acidaminiphila BDBP 071 promoted fenvalerate degradation. When CD-9 was cultured for 16 h before adding BDBP 071, the strain inoculation ratio was 5:5 (v/v), fenvalerate concentration was 75.0 mg/l, fenvalerate was degraded to 84.37 ± 1.25%, and DBP level was reduced by 5.21 mg/l. In addition, 12 fenvalerate metabolites were identified and a pathway for fenvalerate degradation by the cocultured strains was proposed. These results provide theoretical data for further exploration of the mechanisms used by this coculture system to degrade fenvalerate and DBP, and also offer a promising method for effective bioremediation of PPs and their related metabolites in polluted environments.