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1.
目的检测水通道13、在人外周神经肿瘤的表达。方法收集五例患者的神经鞘瘤组织,采用免疫组化方法检测AQP1、AQP3的表达。结果 AQP1、AQP3在神经鞘瘤组织中都有表达,AQP1主要表达在微血管中,AQP3在整个组织中广泛表达。结论首次发现AQP1在神经鞘瘤微血管中表达,可能参与肿瘤血管新生;AQP3在神经鞘瘤细胞广泛表达,可能通过增加肿瘤细胞膜的水通透性而促进肿瘤的生长及浸润。两种水通道蛋白表达量与肿瘤发生发展的关系尚待扩大标本例数结合临床资料进一步分析。  相似文献   

2.
水通道蛋白(AQPs)是近年来研究水液代谢疾病的热点,水通道蛋白-4(AQP4)是美国科学家Agre教授于1994年分离发现的[1],它是水通道蛋白家族的一个成员.迄今为止,已从哺乳动物组织中鉴定中13种AQPs[2].脑组织中的AQP主要为AQP4.AQP4是分布于脑组织中的主要水通道蛋白.  相似文献   

3.
目的 研究氯化钙干预下高脂饮食小鼠的体质量、血脂、血糖、LPS指标变化,应用16S rRNA高通量测序技术检测氯化钙干预下高脂小鼠肠道菌群变化,探索氯化钙通过调节肠道微生物组成对高脂肪饮食诱导的小鼠肥胖的影响.方法 将30只雄性C57BL/6野生型小鼠随机分为对照组(C)、模型组(M)、氯化钙处理组(D),每组10只....  相似文献   

4.
水通道蛋白(AQP)是一种分子量约28 kD的四聚体结构膜通道蛋白。哺乳动物中有13种不同的AQP,表达于不同的组织器官,调节水以及甘油和尿素等小分子跨膜转运。AQP-1主要表达于肾近曲小管和髓袢降支细段上皮细胞顶膜和基底膜,负责肾小管水分子的重吸收。当肾脏发生病变或者损伤时,AQP-1的表达也会随之改变,所以研究AQP-1对于了解水代谢疾病的发生机制以及指导临床水代谢疾病的治疗具有十分重要的意义。  相似文献   

5.
<正>水是生命最基本的组成成分,机体的水平衡对动物的生命维持非常重要。长期以来,人们一直认为水跨生物膜的移动仅靠单纯扩散。但近10余年来大量研究证实机体内广泛存在着特异性的水  相似文献   

6.
目的建立高脂饮食喂养大鼠模型,探讨口服葡萄糖耐量试验(OGTT)和胰岛素耐量试验(ITT),观察其血糖(GLU)动态变化。方法雄性SD大鼠24只,随机分为正常组和高脂组,分别喂养普通饲料和高脂饲料,检测大鼠体质量与血脂,喂养后第2、4、6、8、9周进行OGTT及ITT试验并检测GLU。结果第4周后高脂组体质量显著高于正常组;第10周高脂组体质量高于正常组,差异均有统计学意义(P0.05)。第10周高脂组三酰甘油(TG)、血清总胆固醇(TC)、血压均明显高于正常组,24h尿蛋白定量也高于正常组,差异均有统计学意义(P0.05);高脂组第2周时检测120min OGTT GLU明显高于正常组;第4周90min GLU明显高于正常组;第6周60、90、120min GLU均明显高于正常组;第8周60、120min GLU均明显高于正常组;第9周0、120min GLU均明显高于正常组,差异均有统计学意义(P0.05)。高脂组第4周检测15min ITT GLU明显高于正常组;第6周15、30min ITT GLU明显高于正常组;第8周30min ITT GLU明显高于正常组;第9周15、30min ITT GLU明显高于正常组,差异均有统计学意义(P0.05)。结论高脂饲料喂养周数的增加,高脂组大鼠体质量随高脂饲料的增加而增大,并发生血脂异常,且具有一定程度的胰岛素抵抗。  相似文献   

7.
目的探讨水通道蛋白AQP1、AQP3和AQP5在唾液腺囊肿中表达水平及其意义。方法利用RT-PCR方法对10例正常及囊肿组织各种AQP进行mRNA水平分析。利用Image J软件对RT-PCR进行量化分析。结果AQP1和AQm表达无差异,AQP5表达显著增强。结论AQP5在囊肿中表达增强,提示其可能是参与囊肿形成的主要水通道。其特异性抑制剂的发现,将有助于对于囊肿及干燥综合征发病机制的进一步研究。  相似文献   

8.
近年来,儿童肥胖的发生有上升的趋势,造成肥胖的原因很多,可与摄入热能过多,运动过少,遗传、内分泌失调、心理因素等等有关,尤其与饮食的关系更为突出:  相似文献   

9.
目的观察大黄素对脂肪细胞水通道蛋白-7(AQP7)表达的调节效应并探讨其可能机制。方法成熟的3T3-L1前脂肪细胞分为5组,不同浓度大黄素组(1μM、10μM、50μM),空白对照组(不加药,加入同等体积二甲基亚砜),阳性对照组(吡格列酮10μM)干预24 h。分析大黄素对3T3-L1前脂肪细胞的分化影响,采用MTT法检测12h、24 h、48 h脂肪细胞活力。3T3-L1脂肪细胞诱导分化成熟后构建3T3-L1脂肪细胞胰岛素抵抗模型,分为5组,酶比色法测定甘油及葡萄糖摄取量。用Western Blot分析脂肪细胞中AQP7、过氧化物体增殖剂活化受体γ(PPAR-γ)表达量。结果大黄素组与阳性对照组OD值、3T3-L1脂肪细胞胰岛素抵抗模型甘油及葡萄糖摄取率及脂肪细胞中AQP7与PPAR-γ表达量显著高于空白对照组(P0.05),并且大黄素组呈现剂量依赖性,但大黄素组中浓度与阳性对照组之间无显著性差异(P0.05)。大黄素浓度在1~50μM时,3T3-L1前脂肪细胞活力均≥0.95,且浓度为10μM时,3T3-L1前脂肪细胞活力1。结论大黄素能够促进脂肪细胞分化,增加脂肪细胞同时对甘油及葡萄糖摄取,既能改善胰岛素抵抗又不增加体重,并且存在剂量依赖性。  相似文献   

10.
龚文辉  张素梅  储珏 《中国康复》2016,31(2):114-117
目的:研究8周有氧运动对饮食诱导的肥胖鼠下丘脑和棕色脂肪骨形成蛋白7(BMP7)蛋白表达、下丘脑产热功能调节酶腺苷酸(AMP)依赖的腺苷酸活化蛋白激酶(AMPK)表达,线粒体产热标志物环氧化酶2(COX2)表达的影响,以及机体产热功能的变化情况,探索运动影响棕色脂肪产热功能的机制。方法:SD雄性大鼠采用高脂肪饮食6周制备饮食诱导的肥胖(DIO)模型,分为DIO有氧运动组(EO组)、DIO安静对照组(CO组)和正常安静对照组(C组),3组各10只。DIO有氧运动组予8周(实验第14周)有氧跑台运动干预。免疫印记法检测下丘脑和棕色脂肪BMP 7、COX 2蛋白表达;封闭式流体压力呼吸计检测结算静止代谢率和非颤抖性产热。常规检测体质量、脂体比。结果:实验第6周,EO组及CO组大鼠体质量、脂体比及AMPK蛋白表达均显著高于C组(P0.01),RMR、NST、褐色脂肪BMP 7、COX 2蛋白表达及下丘脑BMP7蛋白表达均明显低于C组(P0.01);实验第14周,EO组大鼠体质量、脂体比及AMPK蛋白表达明显低于CO组(P0.01),RMR、NST、大鼠褐色脂肪BMP 7、COX 2蛋白表达、下丘脑BMP7蛋白表达明显高于CO组(P0.01),AMPK蛋白明显低于CO组(P0.01)。结论:8周有氧运动能够通过增加肥胖鼠下丘脑、棕色脂肪BMP7表达,促进棕色脂肪产热,影响全身能量代谢,减轻体重。  相似文献   

11.
目的研究CXCR7作为一种新的检测指标在乳腺癌的治疗效果及预后判断中的作用。方法应用RT-PCR方法检测乳腺癌癌组织CXCR7基因在新辅助化疗前的表达情况。结果乳腺癌组织中CXCR7表达水平明显高于正常乳腺组织,差异具有统计学意义(P0.05);尽管正常细胞表面很少表达CXCR7分子,但是其细胞内也会表达CXCR7m RNA。CXCR7m RNA在癌组织中的表达量明显高于正常组织,甚至超过20倍,经新辅助化疗后肿块缩小程度与CXCR7表达量呈负相关,即肿块缩小程度越高,预后质量越高,CXCR7表达量越低。结论 CXCR7与乳腺癌的发生、发展及预后有一定的相关性,可能是新辅助化疗的疗效评价指标之一。  相似文献   

12.
Cordyceps militaris is a crude dietary therapeutic mushroom with high nutritional and medicinal values. Mushroom-derived polysaccharides have been found to possess antihyperglycemic and antihyperlipidemic activities. This study aimed to partially clarify the structural characterization and comparatively evaluate hypolipidemic potentials of intracellular- (IPCM) and extracellular polysaccharides of C. militaris (EPCM) in high fat diet fed mice. Results indicated that IPCM-2 is α-pyran polysaccharide with an average molecular weight of 32.5 kDa, was mainly composed of mannose, glucose and galactose with mass percentages of 51.94%, 10.54%, and 37.25%, respectively. EPCM-2 is an α-pyran polysaccharide with an average molecular weight of 20 kDa that is mainly composed of mannose, glucose and galactose with mass percentages of 44.51%, 18.33%, and 35.38%, respectively. In in vivo study, EPCM-1 treatment (100 mg kg−1 d−1) showed potential effects on improving serum lipid profiles of hyperlipidemic mice, reflected by decreasing serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-C) levels by 20.05%, 45.45% and 52.63%, respectively, while IPCM-1 treatment (100 mg kg−1 d−1) remarkably decreased TC, TG and LDL-C levels by 20.74%, 47.93%, and 38.25%, respectively. In addition, EPCM-1 ameliorated hyperlipidemia possibly through upregulating the expression of serum lipoprotein lipase (LPL) and down-regulating the expression of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR), as determined by enzyme-linked immunosorbent assay (ELISA) method, while IPCM-1 remarkably upregulated the expression of serum LPL. This study confirms polysaccharides from C. militaris could be explored as functional foods or natural medicines for preventing hyperlipidemia.

Structural characterization and comparative evaluation of hypolipidemic activities of intracellular and extracellular polysaccharides from Cordyceps militaris.  相似文献   

13.
14.
目的 探讨硫酸锌对高脂喂养载脂蛋白E(AopE)基因敲除小鼠心脏的抗氧化作用.方法 AopE基因敲除小鼠分为高脂模型组、低锌剂量组和高锌剂量组,三组小鼠连续14周喂饲高脂饲料制作动脉粥样硬化模型,除正常对照组和高脂模型组自由饮用去离子水外,其余两组给予高脂饲料喂养的同时分别自由饮用浓度为2.5 mmol/L、25 mmol/L硫酸锌水溶液分别作为低锌剂量组和高锌剂量组.测定小鼠的体重、心重指数、心脏组织的抗氧化能力和金属硫蛋白-Ⅰ型(MT-1)mRNA的表达水平.结果 低锌剂量组和高锌剂量组小鼠的体重和体重增重明显降低(P<0.05);高脂模型组、低锌剂量组和高锌剂量组小鼠心重指数明显高于正常对照组(P<0.05);低锌剂量组和高锌剂量组小鼠的总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)水平均明显高于正常对照组和高脂模型组(P<0.01);但低锌剂量组和高锌剂量组小鼠的丙二醛(MDA)水平明显低于正常对照组和高脂模型组(P<0.01);高锌剂量组小鼠心脏组织中MT-1 mRNA水平明显高于高脂模型组(P<0.05).结论 硫酸锌能够明显增强高脂喂养AopE基因敲除小鼠心脏的抗氧化能力,而MT可能在抗氧化过程中具有重要作用.  相似文献   

15.
Summary. Background: Human eNOS (NOS3) polymorphisms that lower its expression are associated with advanced diabetic nephropathy (DN), and the lack of eNOS accelerates DN in diabetic mice. Diabetes is associated with fibrin deposition. Lack of nitric oxide and fatty acids stimulates the NF‐kB pathway, which increases tissue factor (TF). Objectives: To test the hypothesis that TF contributes to the severity of DN in the diabetic eNOS?/? mice fed a high‐fat diet (HF). Methods: We made eNOS?/? and wild‐type mice diabetic with streptozotocin. Half of them were placed on HF. Results: Blood glucose levels were not affected by either the diet or eNOS genotype. Lack of eNOS in the diabetic mice increased urinary albumin excretion, glomerulosclerosis, interstitial fibrosis, and glomerular basement membrane thickness. HF by itself did not affect DN in the wild‐type mice, but significantly enhanced DN in eNOS?/? mice. More than half of diabetic eNOS?/? mice on HF died prematurely with signs of thrombotic complications. Diabetic kidneys contained fibrin and TF, and their levels were increased by the lack of eNOS and by HF in an additive fashion. The HF diet increased the kidney expression of inflammatory genes. The increase in TF preceded DN, and administration of an anti‐mouse TF antibody to diabetic mice reduced the expression of inflammatory genes. Conclusion: Together, these data indicate a causal link between TF and the exacerbation of DN in eNOS?/? mice. The condition is significantly worsened by enhanced inflammatory responses to an HF diet via TF.  相似文献   

16.
High levels of CD36 expression are found in triglyceride storing and secreting cells such as differentiated adipocytes and mammary secretory epithelial cells and in some capillary endothelial cells. We have found high levels of CD36 in the capillary endothelium of murine adipose tissue and in cardiac and skeletal muscles. Muscle cells themselves were CD36 negative. No CD36 was found in brain endothelium. Cardiac and skeletal muscle tissues are highly oxidative and catabolize long-chain fatty acids as a source of energy while brain tissue does not use long-chain fatty acids for energy production. Since capillary endothelial cell CD36 expression appeared to correlate with parenchymal cell fatty acid utilization and since CD26 has been identified recently as a long-chain fatty acid-binding protein, we examined heart tissue CD36 expression in murine models of insulin-dependent (nonobese diabetic, NOD) and non-insulin-dependent diabetes mellitus (KKAY). Diabetic NOD and KKAY mice had serum triglyceride levels 2.6- and 4.2-fold higher, respectively, than normal mice and exhibited 7- and 3.5-fold higher levels of heart microsomal CD36, respectively, than control mice. Mice fed a 40% fat diet expressed heart tissue CD36 at a level 3.5-fold higher than those fed a 9% fat diet. These data suggest that endothelial cell CD36 expression is related to parenchymal cell lipid metabolism.  相似文献   

17.
目的探讨肾脏20-HETE下调在高脂饮食所致高血压发病机制的作用。方法以高脂饮食喂养3周龄的SD雄性大鼠至12周龄,监浸4正常饮食与高脂饮食两组大鼠的体质量与血压的变化,并以Western blot和HPLC等方法比较两组大鼠的的肾脏各部分20-HETE活性的差异。结果高脂饮食大鼠体质量和MBP在第12周龄明显较正常饮食组增高(414±7)VS(357±5)g,(132±8)VS(108±5)mmHg,P〈0.05),高脂饮食大鼠无论是全肾,还是肾实质各部分的20-HETE活性均明显下降,同时Westernblot表明产生20.HETE的CYP4A表达也出现相应的变化。结论高脂饮食诱导的幼年型肥胖相关性高血压与肾实质的20-HETE下调有关。  相似文献   

18.
目的探讨高脂低碳水化合物膳食模式对肥胖大鼠影响。方法利用膳食模式建立营养性肥胖大鼠模型100只,用随机数字表法按体重分层随机分为普通饲料对照组20只(9.0%脂肪,78%碳水化合物)、高脂饲料组80只(70%脂肪,16%碳水化合物)。每天称进食量;每周称大鼠体重;第3和第11周测血脂;第10周进行口服葡萄糖耐量试验和胰岛素释放试验、第11周测瘦素和酮体。结果两组大鼠原摄食标准为85 g/3 d,对照组大鼠3 d内85 g食物全部食用,观察组大鼠摄食量明显下降,摄入能量减少,且与对照组比较差异有统计学意义(P0.05);观察组大鼠高脂低碳水化合物膳食模式进行第28天、第35天、第42天、第56天、第70 d体重增长明显,且与对照组同时间段比较差异均有统计学意义(P0.05);观察组大鼠高脂低碳水化合物膳食模式进行到第9周后甘油三酯(TG)、总胆固醇(TC)明显高于对照组同期水平、而高密度脂蛋白胆固醇(HDL-C)明显低于对照组,且差异均有统计学意义(P0.05);与对照组比较,观察组大鼠高脂低碳水化合物膳食模式进行70 d后,体重、脂肪垫重、Lee氏指数、脂肪体比等指标明显升高,脾体比明显降低,差异均有统计学意义(P0.05);观察组大鼠观察组在15 min餐后血糖水平明显高于对照组,且与比较差异有统计学意义(P0.05);两组大鼠喂养70 d后瘦素、酮体等指标比较差异无统计学意义(P0.05)。结论高脂低碳水化合物膳食模式使大鼠对脂代谢的调节能力下降,出现血脂紊乱。  相似文献   

19.
目的 探讨外周血单个核细胞(PBMC)IRF-7 mRNA水平与乙肝病毒(HBV)慢性感染的关系.方法 应用实时荧光相对定量RT-PCR法分别检测45例慢性乙型病毒性肝炎(CHB)患者(轻度组、中度组以及重度组各15例)和30例正常对照的PBMC IRF-7 mRNA水平.结果 CHB患者PBMC IRF-7 mRNA表达水平较正常对照组明显下降(P<0.01);IRF-7 mRNA水平由高到低依次为CHB轻度组、中度组、重度组(P<0.01).结论 CHB患者PBMC IRF-7 mRNA水平明显下降,且与疾病严重程度呈正相关,提示可能与乙型肝炎病毒慢性感染有关.  相似文献   

20.
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease spread throughout the world. The most frequent causes of death in NAFLD patients are due both to liver and cardiovascular damage. Several pathways, including the dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway, are involved in the pathogenesis of NAFLD. It has been reported that ADMA plasmatic levels are increased in patients with hepatic dysfunction such as NAFLD. Although many studies demonstrated that some foods are effective in the treatment of NAFLD, few studies have evaluated their effects with respect to the prevention of the disease. It has been reported that sweet orange juice (OJ) consumption may be associated with potential health benefits. However, some varieties of sweet orange are more effective than others. The aim of the present paper was to investigate the effect of blond and blood sweet orange juice in prevention of NAFLD by evaluating its ability to improve liver steatosis in mice with diet-induced obesity, reducing oxidative stress and affecting the DDAH/ADMA pathway. Results obtained in our experimental conditions evidenced that blood orange juice rather than blond orange juice was more effective. Blood orange juice or blond orange juice enriched in anthocyanins may represent a promising dietary option for the prevention of fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease spread throughout the world.  相似文献   

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