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Monascus pilosus-fermented black soybean inhibits lipid accumulation in adipocytes and in high-fat diet-induced obese mice

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Asian Pacific Journal of Tropical Medicine 2015年第4期8卷 276-282页

作者： young-sil lee Bong-Keun Choi Hae Jin lee Dong-Ryung lee Jinhua Cheng Won-Keun lee Seung Hwan Yang Joo-Won Suh Center for Nutraceutical and Pharmaceutical Materials Myongji University Interdisciplinary Program of Biomodulation Myongji University Division of Bioscience and Bioinformatics College of Natural ScienceMyongji University

Objective:To explore the anti-obesity effects and the mechanism of action of Monascus pilosus(***)-fermented black soybean(MFBS)extracts(MFBSE)and MFBS powders(MFBSP)in adipocytes and high-fat diet(HFD)-induced obese mice,***:Black soybean was fermented with ***,and the main constituents in MFBS were analyzed by HPLC *** vitro,MFBSE were examined for anti-adipogenic effects using Oil-Red O *** vivo,mice were fed a normal-fat diet(NFD)control,HFD control or HFD containing 1 g/kg MFBSP for 12 weeks,and then body weight gain and tissues weight ***-time PCR and western blot assay were used to determine the mechanism of anti-adipogenic ***:MFBSE inhibited lipid accumulation in 3T3-L1 adipocytes without exerting cell *** treatment in HFD-fed mice significantly decreased the body weight gain compared with the HFD control *** and MFBSP treatment resulted in significantly lower mRNA levels of adipogenesis-related genes,such as peroxisome proliferator-activated receptorγ(PPARγ),fatty acid-binding protein 4(FABP4),and fatty acid synthase(FAS),in adipocytes and in white adipose tissue(WAT)of HFD-induced obese ***:These results suggest that the anti-obesity effects of MFBS are elicited by regulating the expression of adipogenesis-related genes in adipocytes and WAT of HFDinduced obese mice.

关键词： Monascus pilosus Black soybean Adipocytes High-fat diet-induced obese mice Anti-obesity Adipogenesis-related genes

Roots extracts of Adenophora triphylla *** improve obesity in 3T3-L1 adipocytes and high-fat diet-induced obese mice

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Asian Pacific Journal of Tropical Medicine 2015年第11期8卷 879-886页

作者： Dong-Ryung lee young-sil lee Bong-Keun Choi Hae Jin lee Sung-Bum Park Tack-Man Kim Han Jin Oh Seung Hwan Yang Joo-Won Suh NutraPham Tech Center for Nutraceutical and Pharmaceutical Materials Myongji University Interdisciplinary Program of Biomodulation Myongji University DONG IL Pharmtec Department of Family Medicine.VIEVIS NAMUH Hospital

Objective:To investigate the anti-obesity activity and the action mechanism of the roots of Adenophora triphylla *** extract(ATE) in high-fat diet(HFD)-induced obese mice and 3T3-LI ***:The roots of Ademption triphylla were extracted with 70%*** demonstrate the compounds,linoleic acid was analyzed by using gas chromatography:and the anti-obesity effects and possible mechanisms of ATE were examined in 3T3-L1 adipocytes and HFD-induced obese ***:Treatment with ATE inhibited the lipid accumulation without cytotoxicity in 3T3-L1 ***,200 and 400 mg/kg ATE treatment significantly decreased the body weight gain,white adipose tissues(WATs) weight and plasma triglyceride level,while 100 and 200 mg/kg ATE treatment increased the plasma high-density lipoprotein cholesterol level in the HFD-induced obese mice,as compared with the HFD *** with 200 and 400 mg/kg ATE also lowered the size of adipocytes in adipose tissue and reduced the lipid accumulation in *** treatment showed significantly lower expression level of adipogenesis-relatcd proteins,such as peroxisome proliferator-activated receptor y,fatty acid binding protein(aP2),fatty acid synthase in 3T3-L1 adipocytes;and furthermore,decreased peroxisome proliferatoractivated receptor γ,aP2,fatty acid synthase,sterol regulatory element binding protein-1c,and lipoprotein lipase mRNA expression levels in WAT of the HFD-induced obese ***:These results suggested that the ATE has an anti-obesity effect,which may be elicited by regulating the expression of adipogenesis and lipogenesis-related genes and proteins in adipocytes and WAT of the HFD-induced obese mice.

关键词： Roots of Adenophora triphylla var. japonica extrac

Nobiletin Prevents Body Weight Gain and Bone Loss in Ovariectomized C57BL/6J Mice

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Pharmacology & Pharmacy 2014年第10期5卷 959-965页

作者： young-sil lee Midori Asai Sun-sil Choi Takayuki Yonezawa Toshiaki Teruya Kazuo Nagai Je-Tae Woo Byung-Yoon Cha Research Institute for Biological Functions Chubu University Kasugai Japan Faculty of Education University of the Ryukyus Nishihara Japan Department of Biological Chemistry Chubu University Kasugai Japan Department of Research and Development Erina Co. Inc. Tokyo Japan

Obesity and osteoporosis are associated with estrogen deficiency following menopause. Therefore, it is important to prevent and treat both disorders to maintain a healthy life in postmenopausal women. Nobiletin, a polymethoxylated flavone, exhibits various pharmacologic effects, including anti-tumor and anti-inflammatory activities. Therefore, in this study, we examined the effects of nobiletin on obesity, obesity-related metabolic disorders, and bone mass in ovariectomized (OVX) mice. Mice were divided into four groups and underwent sham operation or OVX. OVX mice were treated with 50 or 100 mg/kg nobiletin, or received vehicle alone (0.3% carboxyl methyl cellulose/0.5% dimethyl sulfoxide). Nobiletin decreased body weight gain and white adipose tissue weight in OVX mice. Nobiletin also decreased triglyceride levels, and tended to reduce plasma total cholesterol and glucose levels. Additionally, nobiletin prevented the reduction in bone mineral density of the trabecular region of the femur in OVX mice. Taken together, our results suggest that nobiletin improves adiposity, dyslipidemia, hyperglycemia, and prevents bone loss in OVX mice. Therefore, nobiletin is expected to have beneficial effects for the prevention and improvement of metabolic disorders and osteoporosis in postmenopausal women.

关键词： Nobiletin Ovariectomy Obesity Lipid and Glucose Metabolism Bone Mineral Density

Cortex cinnamomi extract prevents streptozotocin- and cytokine-induced β-cell damage by inhibiting NF-κB

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World Journal of Gastroenterology 2006年第27期12卷 4331-4337页

作者： Kang-Beom Kwon Eun-Kyung Kim Eun-sil Jeong young-Hoon lee young-Rae lee Jin-Woo Park Do-Gon Ryu Byung-Hyun Park Department of Physiology School of Oriental MedicineWonkwang UniversityIksan 570-749South Korea Department of Oral Anatomy School of DentistryChonbuk National UniversityJeonju 561-756JeonbukSouth Korea Department of Biochemistry Medical SchoolInstitute for Healthcare Technology DevelopmentMedical Research CenterChonbuk National UniversityJeonju 561-756JeonbukSouth Korea

AIM： To clarify the mechanism underlying the antidiabetic activities of cortex cinnamomi extract （CCE）. METHODS： To induce in vivo diabetes, mice were injected with streptozotocin （STZ） via a tail vein （100 mg STZ/kg body weight）. To determine the effects of CCE, mice were administered CCE twice daily for 7 d by oral gavage starting 1 wk before the STZ injection. Blood glucose and plasma insulin concentration were measured as an index of diabetes. Also, to induce cytotoxicity of RINm5F cells, we treated with cytokines （IL-1β （2.0 ng/mL） and IFN-γ （100 U/mL））. Cell viability and nitric oxide production were measured colorimetrically. Inducible nitric oxide synthase （iNOS） mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κβ was assayed by using gel mobility shift assays of nuclear extracts. RESULTS： Treatment of mice with STZ resulted in hyperglycemia and hypoinsulinemia, which was further evidenced by immunohistochemical staining of islets. However, the diabetogenic effects of STZ were completely prevented when mice were pretreated with CCE. The inhibitory effect of CCE on STZ-induced hyperglycemia was mediated through the suppression of iNOS expression. In rat insulinoma RINm5F cells,CCE completely protected against interleukin-1β and interferon-y-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-1β and interferon-y-induced nitric oxide production and in iNOS mRNA and protein expression, and these findings correlated well with in vivo observations. CONCLUSION： The molecular mechanism by which CCE inhibits iNOS gene expression appears to involve the inhibition of NF-κβ activation, These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression,

关键词： Cortex cinnamomi Diabetes Streptozotocin Cytokine NF-κβ

IL-1β activates p44/42 and p38 mitogen-activated protein kinases via different pathways in cat esophageal smooth muscle cells

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World Journal of Gastroenterology 2006年第5期12卷 716-722页

作者： Tai Sang lee Hyun Ju Song Ji Hoon Jeong young sil Min Chang Yell Shin Uy Dong Sohn Department of Pharmacology College of PharmacyChung-Ang UniversitySeoul 156-756Republic of Korea Research Laboratory Dong-A Pharmaceuticals Co.LtdKyunggidoRepublic of Korea

AIM： To examine the pathway related to the IL-1β induced activation of mitogen-activated protein （MAP） kinases in cat esophageal smooth muscle cells. METHODS： Culture of the esophageal smooth muscle cells from cat was prepared. Specific inhibitors were treated before applying the IL-β3. Western blot analysis was performed to detect the expressions of COX, iNOS and MAP kinases. RESULTS： In the primary cultured cells, although IL-β3 failed to upregulate the COX and iNOS levels, the levels of the phosphorylated forms of 1344142 HAP kinase and p38 MAP kinase increased in both concentration- and time-dependent manner, of which the level of activation reached a maximum within 3 and 18 h, respectively. The pertussis toxin reduced the level of p44/42 MAP kinase phosphorylation. Tyrphostin 51 and genistein also inhibited this activation. Neomycin decreased the density of the p44/42 HAP kinase band to the basal level. Phosphokinase C （PKC） was found to play a mediating role in the IL-1β-induced p44/42 MAP kinase activity. In contrast, the activation of p38 MAP kinase was inhibited only by a pretreatment with forskolin, and was unaffected by the other compounds. CONCLUSION： Based on these results, IL-1β-induced p44/42 MAP kinase activation is mediated by the Gi protein, tyrosine kinase, phospholipase C （PLC） and PKC. The pathway for p38 MAP kinase phosphorylation is different from that of p44/42 MAP kinase, suggesting that it plays a different role in the cellular response to IL- 1β.

关键词： IL-1β MAP kinase Esophageal smoothmuscle cells

Oral administration of red ginseng powder fermented with probiotic alleviates the severity of dextran-sulfate sodium-induced colitis in a mouse model

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Chinese Journal of Natural Medicines 2017年第3期15卷 192-201页

作者： JANG Sun-Hee PARK Jisang KIM Sae-Hae CHOI Kyung-Min KO Eun-sil CHA Jeong-Dan lee young-Ran JANG Hyonseok JANG Yong-Suk Department of Molecular Biology and Institute for Molecular Biology and Genetics Chonbuk National UniversityJeonju 54896Korea Department of Bioactive Material Sciences and Research Center of Bioactive Materials Chonbuk National UniversityJeonju 54896Korea Department of Efficacy Research Institute of Jinan Red GinsengJinan 55442Korea Department of Mathematics Sogang UniversitySeoul 04107Korea Department of Oral Maxillofacial Surgery Korea University Ansan HospitalAnsan 15355Korea

Red ginseng is a well-known alternative medicine with anti-inflammatory *** exerts pharmacological effects through the transformation of saponin into metabolites by intestinal *** that intestinal microflora vary among individuals,the pharmacological effects of red ginseng likely vary among *** order to produce homogeneously effective red ginseng,we prepared probiotic-fermented red ginseng and evaluated its activity using a dextran sulfate sodium(DSS)-induced colitis model in *** analysis of intestinal damage indicated that the administration of probiotic-fermented red ginseng significantly decreased the severity of colitis,compared with the control and the activity was higher than that induced by oral administration of ginseng powder or probiotics *** analysis of the levels of serum IL-6 and TNF-α,inflammatory biomarkers that are increased at the initiation stage of colitis,were significantly decreased in probiotic-fermented red ginseng-treated groups in comparison to the control *** levels of inflammatory cytokines and mR NAs for inflammatory factors in colorectal tissues were also significantly decreased in probiotic-fermented red ginseng-treated ***,oral administration of probiotic-fermented red ginseng reduced the severity of colitis in a mouse model,suggesting that it can be used as a uniformly effective red ginseng product.

关键词： Colitis Fermentation Inflammation Probiotics Red ginseng

Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils

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Neural Regeneration Research 2017年第9期12卷 1458-1464页

作者： Jae-Chul lee Jeong-Hwi Cho Tae-Kyeong lee In Hye Kim Moo-Ho Won Geum-sil Cho Bich-Na Shin In Koo Hwang Joon Ha Park Ji Hyeon Ahn Il Jun Kang young Joo lee Yang Hee Kim Department of Neurobiology School of Medicine Kangwon National University Department of Pharmacology & Toxicology Shinpoong Pharmaceutical Co. Ltd. Department of Physiology College of Medicine Hallym University Department of Anatomy and Cell Biology College of Veterinary Medicine and Research Institute for Veterinary Science Seoul National University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Department of Food Science and Nutrition Hallym University Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Department of Surgery School of Medicine Kangwon National University

Calbindin D-28K （CB）, a Ca2＋-binding protein, maintains Ca2＋ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We inves- tigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei （NeuN） and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia （39.5 ＋ 0.2~C） was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neu- ronal damage/death in the pyramidal layer of CA1-3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreac- tivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.

关键词： nerve regeneration hyperthermic condition ischemia/reperfusion injury subregions of hippocampus delayed neuronal death calbindin D-28k neural regeneration

Brain metabolism in patients with vegetative state after post-resuscitated hypoxic-ischemic brain injury： statistical parametric mapping analysis of F-18 fluorodeoxyglucose positron emission tomography

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Chinese Medical Journal 2013年第5期126卷 888-894页

作者： Yong Wook Kim Hyoung Seop Kim young-sil An Department and Research Institute of Rehabilitation Medicine Yonsei University College of Medicine Seoul Republic of Korea Department of Physical Medicine and Rehabilitation NationalHealth Insurance Corporation Ilsan Hospital Gyonggi-doRepublic of Korea Department of Nuclear Medicine Ajou University School ofMedicine Suwon Republic of Korea

Background Hypoxic-ischemic brain injury （HIBI） after cardiopulmonary resuscitation is one of the most devastating neurological conditions that causing the impaired consciousness. However, there were few studies investigated the changes of brain metabolism in patients with vegetative state （VS） after post-resuscitated HIBI. This study aimed to analyze the change of overall brain metabolism and elucidated the brain area correlated with the level of consciousness （LOC） in patients with VS after post-resuscitated HIBI. Methods We consecutively enrolled 17 patients with VS after HIBI, who experienced cardiopulmonary resuscitation. Overall brain metabolism was measured by F-18 fluorodeoxyglucose positron emission tomography （F-18 FDG PET） and we compared regional brain metabolic patterns from 17 patients with those from 15 normal controls using voxel-by-voxel based statistical parametric mapping analysis. Additionally, we correlated the LOC measured by the JFK-coma recovery scale-revised of each patient with brain metabolism by covariance analysis. Results Compared with normal controls, the patients with VS after post-resuscitated HIBI revealed significantly decreased brain metabolism in bilateral precuneus, bilateral posterior cingulate gyrus, bilateral middle frontal gyri, bilateral superior parietal gyri, bilateral middle occipital gyri, bilateral precentral gyri （PFEw correctecd 〈0.0001 ）, and increased brain metabolism in bilateral insula, bilateral cerebella, and the brainstem （PFEWcorrectecd 〈0.0001 ）. In covariance analysis, the LOC was significantly correlated with brain metabolism in bilateral fusiform and superior temporal gyri （P uncorrected 〈0.005）. Conclusions Our study demonstrated that the precuneus, the posterior cingulate area and the frontoparietal cortex, which is a component of neural correlate for consciousness, may be relevant structure for impaired consciousness in patient with VS after post-resuscitated HIBI. In post-resuscitated HIBI, measuremen

关键词： hypoxic-ischemic brain injury vegetative state brain metabolism

Signal transduction of bombesin-induced circular smooth muscle cell contraction in cat esophagus

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World Journal of Gastroenterology 2006年第14期12卷 2259-2263页

作者： Sung-Uk Park Chang-Yell Shin Jung-Su Ryu Hyen-O La Sun-young Park Hyun-Ju Song young-sil Min Dong-Seok Kim Uy-Dong Sohn Department of Pharmacology College of Pharmacy Chung Ang UniversitySeoul 156-756Republic of Korea Department of Pharmacology College of Pharmacy Chung Ang UniversitySeoul 156-756Republic of Korea Research LaboratoryDong-A Pharm. Co. LtdYongin 449-905Kyunggi-DoRepublic of Korea Department of Pharmacology College of Medicine The Catholic University of KoreaSeoul 137-701Republic of Korea Research Division for Human Life Sciences Seoul National University 28 Yongon-DongChongno-GuSeoul 110-744Republic of Korea

AIM： To investigate the mechanism of bombesin-induced circular smooth muscle cell contraction in cat esophagus. METHODS： Specific G protein or phospholipase C involved in cat esophagus contraction was identified, muscle cells were permeabilized with saponin. After per- meabilization of muscle cells, the Gi3 antibody inhibited bombesin-induced smooth muscle cell contraction. RESULTS： Incubation of permeabilized circular muscle cells with PLC-β3 antibody could inhibit bombesin-induced contraction. H-7, chelerythrine （PKC inhibitor） and genistein （protein tyrosine kinase inhibitor） inhibited bombesin-induced contraction, but DAG kinase inhibitor, R59949, could not inhibit it. To examine which mitogen-activated protein kinase （MAPK） was involved in bombesin-induced contTaction, the specific MAPK inhibitors （MEK inhibitor, PD98059 and p38 MAPK inhibitor, SB202190） were used. Preincubation of PD98059 blocked the contraction induced by bombesin in a concentration-dependent manner. However, SB202190 had no effects on contraction. CONCLUSION： Bombesin-induced circular muscle cell contraction in cat esophagus is mediated via a PKC or a PTK-dependent pathway or p44/p42 HAPK pathway.

关键词： Bombesin G protein Phospholipase C Protein kinase C Protein tyrosine kinase MAP Kinase Cell contraction