检索结果-南通市图书馆

11 beta-hydroxysteroid dehydrogenase type 1 promotes differentiation of 3T3-L1 preadipocyte

Acta Pharmacologica Sinica 2007年第8期28卷 1198-1204页

作者： Yun LIU~(2,3,4) Yan SUN~(2,4) Ting ZHU~2 Yu XIE~2 Jing YU~2 Wen-lan SUN~2 Guo-xian DING~(2,5) Gang HU~(3,5) ~2department of Geratology the First Affiliated Hospital,nanjing medical university,nanjing 210008,china ~3department of pharmacology,nanjing medical university,nanjing 210029,china department of Geratology the First Affiliated Hospital Nanjing Medical University Nanjing China department of pharmacology Nanjing Medical University Nanjing China

Aim:To investigate the relationship between 11 beta-hydroxysteroid dehydroge-nase type 1(1 lbeta-HSD1),a potential link between obesity and type 2 diabetes,and preadipocyte ***:Mouse 1 lbeta-HSD 1 siRNA plasmidswere transfected into 3T3-L1 preadipocytes(a cell line derived from mouseSwiss3T3 cells that were isolated from mouse embryo),for examination of theeffect of targeted 11 beta-HSD 1 inhibition on differentiation of 3T3-L 1 ***-ferentiation was stimulated with 3-isobutyl-l-methyxanthine,insulin,*** transcription level of the genes was detected by ***:Lipid accumulation was significantly inhibited in cells transfectedwith mouse 1 lbeta-HSD1 siRNA compared with non-transfected 3T3-L1 *** lipid droplets were detected in the transfected cells both prior to stimulationand after stimulation with differentiation-inducing *** expression ofadipocyte differentiation-associated markers such as lipoprotein lipase and fattyacid synthetase were downregulated in the transfected ***,the expres-sion of preadipocyte factor-1,an inhibitor of adipocyte differentiation,wasdownregulated upon stimulation of differentiation and had no changes in thetransfected ***:11 beta-HSD1 can promote *** on this,we propose that 11 beta-HSD1 may be an importantcandidate mediator of obesity and obesity-induced insulin resistance.

关键词： 11 beta-hydroxysteroid dehydrogenase type 1 siRNA 3T3-L1 cell differentiation obesity

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Role of 11-beta-hydroxysteroid dehydrogenase type 1 in differentiation of 3T3-L1 cells and in rats with diet-induced obesity

引用

Acta Pharmacologica Sinica 2006年第5期27卷 588-596页

作者： Yun LIU~(2,3) Wen-lan SUN~3 Yan SUN~3 Gang HU~(2,4) Guo-xian DING~(3,4) ~2department of Pharmaeology,nanjing medical university,nanjing 210029,china ~3department of Geratology,the First Hospital Affiliated to Nan jinx,medical university,nanjing 210008,china department of pharmacology Nanjing Medical University Nanjing China department of Geratology the First Hospital Affiliated to Nanjing Medical University Nanjing China

Aim:To observe the roles of 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in in vitro preadipocyte differentiation and in rats with diet-induced obe-sity (DIO).Methods:Protein expression of 11β-HSD1 in the process of 3T3-L1 celldifferentiation and in various tissues of the rats were detected by Western blotanalysis;expression of 11β-HSD1 mRNA and glucocorticoid receptor (GR) andother marker genes of preadipocyte differentiation were detected by using real-time ***:Lipid droplets in 3T3-L1 cells accumulated and increased afterstimulation.A dramatically elevated protein level of 11β-HSD1,especially in thelate stages of 3T3-L1 cell differentiation,was *** relative mRNA levelsof 11β-HSD1,GR and cell differentiation markers LPL,aP2,and FAS wereupregulated,and Pref-1 was downregulated during the *** DIO rats,bodyweight,visceral adipose mass index and the protein expression of 11β-HSD1increased,especially in adipose tissue,brain and *** insulin,triglyceride,total cholesterol and low-density lipoprotein cholesterol were foundto be increased in DIO rats,but without any obvious changes in blood glucose ortumor necrosis factor-α ***:11β-HSDI may promote preadipocytedifferentiation,and may be involved in the development of obesity.

关键词： 11-beta-hydroxysteroid dehydrogenase type 1 glucocorticoids adipocytes cell differentiation obesity

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

6-Hydroxydopamine-induced glutathione alteration occurs via glutathione enzyme system in primary cultured astrocytes

引用

Acta Pharmacologica Sinica 2005年第7期26卷 799-805页

作者： Ji ZHANG Jun HU Jian-hua DING Hong-hong YAO Gang HU~2 department of pharmacology,nanjing medical university,nanjing 210029,china department of pharmacology Nanjing Medical University Nanjing China

Aim:To define the role of enzymes involved in glutathione metabolism in 6-hydroxydopamine(6-OHDA)-induced glutathione alteration in primary ***:Total glutathione(GSx)levels were determined using themodified enzymatic microtiter plate *** mRNA levels of γ-glutamylcysteinesynthetase(γGCS),γ-glutamyltransferase(γGT),glutathione peroxidase(GPx),GR(glutathione reductase),and glutathione transferases(GST)were determined us-ing RT-PCR.γGT activity was determined using 7GT assay ***:Inprimary cultured astrocytes,6-OHDA induced a significant elevation of cellularGSx levels after treatment for 24 ***,the GSx levels decreased after 24 hand the values were even lower than the value in the control group without 6-OHDA at 48 ***-PCR data showed that the mRNA levels of γGCS,the rate-limiting enzyme of γ-L-glutamyl-L-cysteinylglycine(GSH)synthesis,were increasedby 6-OHDA after treatment for 24 h and 48 h;the mRNA levels of GPx,GR,and GSTdid not alter in 6-OHDA-treated astrocytes after treatment for 24 h and 48 h;and 6-OHDA increased the mRNA levels and the activity of TGT after treatment for 48 h,which induced a decrease in GSx levels,despite the up-regulation of γCS afterexposure to 6-OHDA for 48 ***:The change in γGCS correlated withthe increase in GSH levels induced by 6-OHDA after treatment for 24 *** levelsdecreased because of increased γGT mRNA levels and γGT activity induced by 6-OHDA after treatment for 48 h.

关键词： 6-hydroxydopamine glutathione oxidative stress glutamate-cysteine ligase gammaglutamyltransferase

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Proteomic response analysis of endothelial cells of human coronary artery to stimulation with carbachol

引用

Acta Pharmacologica Sinica 2004年第9期 22-28页

作者： Min YU, Dong-mei CHEN, Gang HU, Hai WANGBeijing Institute of pharmacology and Toxicology, Beijing 100850, china department of pharmacology and Neurobiology, nanjing medical university, nanjing 210029,china

AIM: To identify the molecular basis of the endothelial target for acetylcholine (ETA). METHODS: Proteomic methods were used to monitor changes in protein expression in the first 10 h following the stimulation of human coronary endothelial cells with carbachol 100 μmol/L. Thirty proteins showing the largest changes were identified by mass spectrometry. RESULTS: Based on analysis with Image Master 2-D

关键词： endothelium carbachol human coronary artery endothelial cells proteome two-dimensional gel electrophoresis protein identification

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Protective effects of bendazac lysine on early experimental diabetic nephropathy in rats

引用

Acta Pharmacologica Sinica 2005年第6期26卷 721-728页

作者： Xiao-xing YIN~1, Yin-di ZHANG~(1,2), Jian-ping SHEN~1, Hai-wei WE~3, Xiang ZHU~3, Li-min LI~1, Jun QIU~1, Shao-jun JIANG~4, Xiao-gang ZHENG~4 ~1 department of pharmacology and ~3 department of Pathogenic Biology, nanjing medical university, nanjing, 210029 ~4 department of Pathology, nanjing Jing Ling Hospital, nanjing 210002, china department of pharmacology Nanjing Medical University Nanjing China department of Pathogenic Biology Nanjing Medical University Nanjing China department of Pathology Nanjing Jing Ling Hospital Nanjing China

Aim: To investigate the preventive and protective effects of bendazac lysine (BDL) on experimental early diabetic nephropathy (DN) rats. Methods: After an early DN model was induced by streptozotocin, rats were administered BDL at doses of 100,200, and 400 mg/kg for 8 weeks. Blood glucose, microalbuminuria, kidney index, total antioxidative capacity, laminin, advanced glycation end products (AGE), aldose reductase (AR) activity, and the relative quantity of transforming growth factor 1 (TGF-1) mRNA were measured by different methods. The ultrastructural morphology was observed by transmission electron microscope. Results: The physical behaviors of early DN rats were hypopraxia, cachexia, and polyuria, while those treated with high doses of BDL were vibrant and vigorous. For BDL-treated DN rats, when compared with vehicle-treated DN rats, the blood glucose level and the intensity of oxidative stress were ameliorated. Also, the microalbuminuria level, AGE either in serum or in renal, and AR activity were significantly reduced. Furthermore, the expression of TGF-1 mRNA in the kidney cortex was declined and the thickness of glomerular base membrane was decreased significantly. The ultrastructure of glomerulus and mesangial matrix of BDL-treated DN rats were ameliorated. Conclusion: BDL has protective effects on several pharmacological targets in the progress of DN and is a potential drug for the prevention of early DN.

关键词： bendazac lysine diabetic nephropathies blood glucose oxidative stress

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Protective effects of iptakalim,a novel ATP-sensitive potassium channel opener,on global cerebral ischemia-evoked insult in gerbils

引用

Acta Pharmacologica Sinica 2006年第6期27卷 665-672页

作者： Hua CHEN~(2,4)Yong YANG~(2,4)Hong-hong YAO~2 Xing-chun TANG~2 Jian-hua DING~2 Hai WANG~3 Gang HU~(2,5)2 Laboratory of Neuropharmacology,department of Anatomy,Histology and pharmacology,nanjing medical university,nanjing 210029,china 3 department of Cardiovascular pharmacology,Beijing Institute of pharmacology and Toxicology,Beijing 100850,china department of Anatomy Laboratory of Neuropharmacology Histology and Pharmacology Nanjing Medical University Nanjing China department of Cardiovascular pharmacology Beijing Institute of Pharmacology and Toxicology Beijing China

Aim:To investigate the protective role of iptakalim,a novel ATP sensitive potas-sium channel opener,on global cerebral ischemia-evoked insult in gerbils andglutamate-induced PC 12 cell ***:Global cerebral ischemia was in-duced by occluding the bilateral common carotid arteries in gerbils for 5 *** field maze and T-maze were employed to investigate the experimental thera-peutic value of iptakalim on ischemic brain insult（n=8）.The pyramidal cells in thehippocampal CA1 regions were counted to assess the protective effects *** released from the gerbil hippocampus and PC12 cells weredetermined by *** calcium was measured by Fluo-3 AM with ABio-Rad Radiance 2100TM confocal system in conjunction with a Nikon *** glutamate uptake measurements were determined by liq-uid scintillation ***:Iptakalim（0.5-4.0 mg/kg per day,ip）couldreduce the high locomotor activity evoked by ischemia and improve global cere-bral ischemia-induced working memory *** studies revealedthat iptakalim could increase the survival neuron in the hippocampus CA1 zone ina dose-dependent ***,iptakalim could reverse ischemia-evokedincreases of glutamate in the hippocampus of *** an in vitro study,iptakalimprotected PC12 cells against glutamate-induced excitotoxicity,reduced the[Ca2+]iincreases,and enhanced the glutamate uptake activity of primary ***:Iptakalim plays a key role in preventing global cerebralischemia-evoked insults in gerbils and glutamate-induced PC12 cell injury by *** might be a promising novel candidate for the preventionand/or treatment of stroke.

关键词： ATP-sensitive potassium channel opener iptakalim global cerebral ischemia neuroprotection excitotoxicity

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Influences of Chloropazine, Nimodipine and Their Combination on the Toxic Effects of Cadmium in Liver and Kidney of Mice

引用

Biomedical and Environmental Sciences 1999年第3期12卷 212-221页

作者： TANG LINC-FANG YANG YONC-NIAN CHEN YAN-MENG ZHANG ZHEN-LING SONG LINGAND FENG ZHI-YING(department of Toxicology, nanjing medical university, 140 Hanzhong Road,nanjing 210029, china) 南京医科大学毒理学系江苏南京 210029 南京医科大学毒理学系江苏南京

The influences of the calmodulin antagonist chlorpromazine (CPZ), and calcium channel blocker nimodipine (NIMO) and their combination on cadmium (Cd) poisoning of mice were studied. A seties of biochemical parameters including urinary enzyme activities, blood and urine Cd levels, metallothionein (MT) contents in liver and kidney, hepatic ultrastructure and Ca2+ -Mg2+ AT-Pase activity in erythrocyte membrane were determined. Animal models for Cd poisoning were established by peritoneal injection of 1/5 LD50 CdCl2. The experimental groups were protected by administration of CPZ, NIMO and CPZ and NIMO in combination l h before the injection of CdCl2. Five days later, samples were collected for analysis. The data showed that Crs could protect kidney tissue against Cd-induced damage, as the urinary γ-glutamyl traspepti dase (γ- GT ) and N- acetyl-β-D-glucosaminidase (NAG) activities were reduced significantly. There was neither evidence of the protective effect of NIMO on kidney tissue nor an indication of a synergistic effecf of Crs and *** CPZ and NIMO showed a considerable protective effect against the deerease in Ca2+ -Mg2+ AT-Pase activity, and a synergistic action was observed. Cd content in blood was reduced significanily by CPZ or the combination of CPZ and NIMO, but elevated by NIMO. Both CPZ and NIMO consideraby increased MT contents in livers and kidneys and ameliorated damaged to the hepatic ultrastructures caused by Cd. The results indicated that these inhibitors could protect mice against the toxic effects of Cd in liver and kidney tissues, while CPZ was more efficient than NIMO. The combination of CPZ and NIMO exerted a synergistic action. The protective action of these two drugs might be relevent to the function of MT.

关键词： Influences of Chloropazine Nimodipine and Their Combination on the Toxic Effects of Cadmium in Liver and Kidney of Mice

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Dispersion of ventricular mRNA of RyR2 and SERCA2 associated with arrhythmogenesis in rats

引用

Acta Pharmacologica Sinica 2004年第6期25卷 36-41页

作者： Hong-lan WANG, De-zai DAI2, Feng GAO3, Yan-pin ZHANG3, Feng LU Research Division of pharmacology, china Pharmaceutical university, nanjing 210009, china 3Laboratorial Center ofMedicine, Southeast university, nanjing 210009, china Research Division of pharmacology China Pharmaceutical University Nanjing 210009 Laboratorial Center of Medicine Southeast University Nanjing 210009

AIM: To investigate the effect of CPU86017 on the changes of mRNA abundance of different calcium handling system in infarcted heart. METHODS: Rats were subjected to left coronary ligation to induce myocardial infarc- tion (MI). The treatment with either propranolol (Pro) 5 mg/kg ip or CPU86017 1, 2, and 4 mg/kg ip was initiated on the next day of operation and continued for 20 d. Medication with isoproterenol (Isop) 3 mg/kg sc started on the d 17-21. Ventricular mRNA abundance of ryanodine receptor 2 (RyR2), sarcoplasmic reticulum Ca2+-ATPase (SERCA2), L-type Ca2+ channel, and Na+/Ca2+exchanger (NCX1) were measured. RESULTS: Arrhythmic scores (AS) in the Isop group was raised up to 5.27±1.75 (P3. The AS was depressed by Pro (1.63±1.53, P3.00±1.24, and 1.70±1.85, P<0.01 vs Isop). The significant dispersion of depressed mRNA abundance of RyR2 and SERCA2 was associated with an increase in AS in Isop group, and it was much depressed in the left than the right ventricle. The dispersion and depression of mRNA were restored significantly by Pro and CPU86017, asso- ciated with suppression on AS. In Isop group, the mRNA abundance of L-type Ca2+ channel was not changed; and a moderate increase in the mRNA of NCX1 was seen, the changes were regressed by Pro and CPU86017. CONCLUSION: Isop-induced arrhythmogenesis in MI heart was correlated mainly with a dispersion of depressed mRNA abundance in ventricle likely due to the consequence of PKA over-phosphorylation. A suppression of arrhythmia by Pro and CPU86017 resulted from a regression of the dispersion and depression of RyR2 and SERCA2.

关键词： myocardial infarction isoproterenol arrhythmia calcium 4-chlorobenzyltetrahydroberberine

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Modulation of P-glycoprotein function by amlodipine derivatives in brain microvessel endothelial cells of rats

引用

Acta Pharmacologica Sinica 2005年第2期26卷 166-170页

作者： Bian-sheng JI Ling HE Guo-qing LIU department of pharmacology,china Pharmaceutical university,nanjing 210009,china department of pharmacology China Pharmaceutical University Nanjing China

Aim:To investigate whether the amlodipine derivatives,CJX1 and CJX2,havea modulative effect on P-glycoprotein(P-gp)function in rat brain microvesselendothelial cells(RBMEC).Methods:Isolated RBMEC were cultured in DMEM/F 12(1:1)*** amount of intracellular rhodamine(Rh123)was determined,using a fluorescence spectrophotometer,to evaluate the function of ***:The accumulation of Rh123 in RBMEC was potentiated in a concentration-dependent manner after incubation with CJX1 and CJX2 at 1,2.5,5,and 10μmol/L(P3 was observed in human umbili-cal vein endothelial cells after incubation with CJX1 and CJX2 10 μmol/L(P>0.05).Accumulation of intracellular Rh123 was increased and efflux of intra-cellular Rh123 was decreased in a time-dependent manner from 0-100 min afterCJX1 and CXJ2 at 10 ∴mol/L *** inhibitory effect of CJX1 and CJX2on P-gp function was reversible and remained even at 120 min after removal ofCJX1 and CJX2 at 2.5μmol/L from the ***:CJX1 and CJX2exhibited a potent effect in the inhibition of P-gp function in vitro.

关键词： amlodipine derivatives CJX1 CJX2 verapamil P-glycoprotein blood brain barrier vascular endothelium

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Sodium ferulate prevents amyloid-beta-induced neurotoxicity through suppression of p38 MAPK and upregulation of ERK-1/2 and Akt/protein kinase B in rat hippocampus

引用

Acta Pharmacologica Sinica 2005年第8期26卷 943-951页

作者： Ying JIN~2, En-zhi YAN~3, Ying FAN~3, Zhi-hong ZONG~4, Zhi-min QI~3, Zhi LI~(2,5) ~2department of Ethnopharmacology, china medical university, Shengyang 110001, china ~3department of pharmacology, Jinzhou medical College, Jinzhou 121001, china ~4department of Biochemistry, china medical university Shengyang 110001, china department of Ethnopharmacology China Medical University Shengyang China department of pharmacology Jinzhou Medical College Jinzhou China department of Biochemistry China Medical University Shengyang China

Aim: To observe whether an amyloid β （Aβ）-induced increase in interleukin （IL）-1β was accompanied by an increase in the p38 mitogen-activated protein kinase （MAPK） pathway and a decrease in the cell survival pathway, and whether so-dium ferulate （SF） treatment was effective in preventing these Aβ-induced changes. Methods: Rats were injected intracerebroventricularly with Aβ25-35. Seven days after injection, immunohistochemical techniques for glial fibrillary acidic protein （GFAP） were used to determine the astrocyte infiltration and activation in hippo-campal CA1 areas. The expression of IL-1β, extracellular signal-regulated kinase （ERK）, p38 MAPK, Akt/protein kinase B （PKB）, Fas ligand and caspase-3 were determined by Western blotting. The caspase-3 activity was measured by clea-vage of the caspase-3 substrate （Ac-DEVD-pNA）. Reverse transcription-polymerase chain reaction was used to analyze the changes in IL- 1βmRNA levels. Results:Intracerebroventricular injection of Aβ-（25-35） elicited astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by increased IL-1β production and elevated levels of IL-1β mRNA. Increased IL-1β synthesis was accompanied by increased activation of p38 MAPK and downregulation of phospho-ERK and phospho-Akt/PKB in hippocampal CA regions prepared from Aβ-treated rats, leading to cell death as assessed by activa-tion of caspase-3. SF significantly prevented Aβ-induced increases in IL-Iβ and p38 MAPK activation and also Aβ-induced changes in phospho-ERK and phospho-Akt/PKB expression levels. Conclusion: SF prevents Aβ-induced neu-rotoxicity through suppression of p38 MAPK activation and upregulation of phospho-ERK and phospho-Akt/PKB expression.

关键词： ferulic acid amyloid interleukin-1 p38 mitogen-activated protein kinases extra-cellular signal-regulated kinases proto-oncogene proteins c-akt Alzheimer disease

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：