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1.
抵抗素是一种与肥胖以及肥胖相关疾病密切相关的脂肪细胞因子.近年研究表明,该因子参与炎症的发生过程.文章从抵抗素与炎症因子和C反应蛋白的相关性,与内皮细胞的相互作用以及炎症相关的临床和试验研究几个方面阐述了抵抗素与炎症的关系.  相似文献   
2.
取单层培养72 h生长良好的犊牛肝细胞,采用单因素重复试验,分别添加0、25、50、100、200、400 ng/L的牛重组抵抗素(resistin),每个处理3个重复(每重复2孔).继续培养12 h后分别提取RNA并制备细胞上清液.应用荧光定量PCR方法检测牛重组Resistin对肝细胞糖异生关键酶丙酮酸羧化酶(Pyruvate carboxylase,PC)基因表达的影响,同时用比色法检测其对肝细胞PC酶活性的影响.结果表明,一定浓度的resistin显著下调了肝细胞PCmRNA表达,且降低了PC酶活性.  相似文献   
3.
The aim of the present study was to compare the expression of adipose tissue mRNA related to glucose metabolism between Japanese Black steers (n = 5) and Holstein steers (n = 5). We examined the expression of the resistin, tumor necrosis factor‐α (TNF‐α), glucose transporter 1 (GLUT1) and growth hormone receptor (GHR) genes using real‐time polymerase chain reaction of cDNA in adipose tissue. The cDNA sequence identified by 5′/3′‐rapid amplification of cDNA and the deduced amino acid sequence were highly conserved in human, porcine and murine resistin. Expression of resistin mRNA was significantly greater in Holstein steers than in Japanese Black steers. In contrast, expression of TNF‐α mRNA was slightly greater in Japanese Black steers. Expression of GHR mRNA was significantly greater in Japanese Black steers compared with the Holstein steers, although there was no significant difference in the expression of GLUT1 mRNA. However, the plasma non‐esterified fatty acid (NEFA), glucose, insulin and growth hormone concentrations did not differ between Japanese Black and Holstein steers. The present results show that there is a difference in the expression level of mRNA related to glucose metabolism between Japanese Black steers and Holstein steers.  相似文献   
4.
旨在探究牛抵抗素通过TLR4/MyD88非依赖信号通路诱发牛肺泡巨噬细胞的相关炎症反应机理。使用100 ng·mL-1终浓度牛抵抗素诱导牛肺泡巨噬细胞,分别在0、1.5、3.0、6.0、12.0、24.0 h时采用qRT-PCR检测TLR4/MyD88非依赖信号通路相关基因(TLR4、TRAMNF-κB)mRNA水平表达量,通过ELISA法检测下游IL-6、1L-1β、TNF-α等促炎细胞因子表达水平。结果显示,100 ng·mL-1牛抵抗素处理牛肺泡巨噬细胞后,TLR4、TRAMNF-κB基因表达量于6.0 h时极显著上调(P<0.01),诱导12.0 h时,相关基因表达量达到最高;IL-6、1L-1β、TNF-α等促炎细胞因子于1.5 h表达量极显著上调(P<0.01),且均存在时间依赖效应。抵抗素诱导牛肺泡巨噬细胞后,可激活TLR4/MyD88非依赖信号通路,通过信号传递,释放大量促炎细胞因子,引起肺部炎症。  相似文献   
5.
抵抗素是一种脂肪因子,被证明与胰岛素抵抗密切相关,但其作用机制尚不明确。近年研究表明抵抗素参与了肥胖有关的炎症进程,对胰岛素敏感组织(脂肪、肝脏)炎症状态起到重要调控作用。肥胖诱导的慢性低度炎症是导致机体胰岛素抵抗的重要因素,抵抗素通过对炎症的调控参与肥胖机体胰岛素抵抗的发生。本文主要从组织及分子层面探讨抵抗素诱导胰岛素抵抗的炎症机制,为进一步了解抵抗素在肥胖相关疾病病理机制中的作用提供一些思路。  相似文献   
6.
Abstract: In addition to its role as an energy storage depot, adipose tissue is now recognized as a complex endocrine organ. Adipose tissue releases a variety of factors, termed adipokines, that regulate energy metabolism, cardiovascular function, reproductive status, and immune function. Some of the better‐studied adipokines include leptin, adiponectin, and components of the renin‐angiotensin system such as angiotensinogen. The function of more recently discovered adipokines such as resistin are under intense scrutiny. Abnormal production or regulation of adipokines occurs in obese individuals and is implicated in the development of a variety of associated co‐morbidities including metabolic syndrome, type 2 diabetes, atherosclerosis, heart disease, and cancer in people, although evaluation in domestic species is just beginning. Adipokines are now being examined as potential biomarkers for risk assessment for development of complications related to obesity. This article summarizes the function and regulation of some better‐characterized adipokines. It also reviews the current information on the characterization of adipokines in some domestic species in which rates of obesity and obesity‐related disorders are increasing, such as the dog, cat, and horse.  相似文献   
7.
应用PCR技术从含有猪resistin基因(Retn)cDNA的质粒pMD18T-Retn中扩增Retn基因片段,将其克隆至pcDNA3.1( )表达载体中,构建重组表达质粒pcDNA3.1-Retn。采用LipofectaminTM2000转染Hela细胞,用G418筛选稳定表达的Hela细胞株。用RT-PCR、Tricine-SDS-PAGE和Western blot技术检测,结果表明Retn基因在Hela细胞中得到转录与表达。  相似文献   
8.
抵抗素的研究备受关注,是RELMs家族成员,与糖代谢、脂肪代谢、胰岛素抵抗等有很大关系。年龄、性别、营养状况、激素、各种细胞因子都对抵抗素mRNA的表达具有调节作用,奶牛抵抗素的研究目前也受到重视。  相似文献   
9.
抵抗素引起胰岛素抵抗机制的研究进展   总被引:3,自引:0,他引:3  
抵抗素是存在于血浆中的富含半胱氨酸的分泌性蛋白,其分子内二硫键的形成对于维系它的空间构象及生物活性非常重要.许多报道认为抵抗素可以引起胰岛素抵抗,它的发现为与胰岛素抵抗相关的疾病肥胖和2型糖尿病提供了一个新的研究方向,但其引起胰岛素抵抗的机制至今不是很明确.文章介绍了抵抗素的结构特点及其引起胰岛素抵抗的机制.  相似文献   
10.
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