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1.
目的:观察电针对高脂饮食诱导的肥胖大鼠脂质蓄积对改善瘦素抵抗的影响.方法:选用3周龄SD雄性大鼠42只,随机分为2组:正常组(n=6),普通饲料喂养,高脂组(n=36),高脂饲料喂养.12周后将高脂组造模成功的大鼠(n=18)随机分为模型组、电针组和假针刺组.测定各组大鼠体质量、脂肪质量、血脂、瘦素等相关指标,qPCR检测各组大鼠下丘脑瘦素受体的mRNA表达变化,用HE染色观察比较各组大鼠肝脏的形态学差异.结果:与正常组比较,高脂模型组体质量显著升高(P<0.01),显示肥胖大鼠造模成功.与模型组相比,电针组大鼠的体质量、内脏脂肪量、TG、TCL、leptin均显著降低(P<0.05),下丘脑瘦素受体mRNA表达量显著上升(P<0.01).HE染色结果显示,电针组大鼠肝脏内的脂滴空泡较模型组明显减少,形态恢复与正常组接近.假针刺组大鼠除项后脂肪量外其他各项指标与模型组相比无明显差异(P>0.05).结论:电针可以减少肥胖大鼠脂质堆积并改善瘦素抵抗,具有一定的抑制肥胖效果.  相似文献   

2.
目的:研究荜茇-13味对大鼠非酒精性脂肪肝病的疗效.方法:雄性Wister大鼠40只随机分组,每组8只.正常对照组仅喂饲普通饲料,其他大鼠喂饲高脂饲料(88%标准普通饲料+10%猪油+2%胆固醇)12周.分为模型对照组和荜茇-13味低(2mg/kg)、中(4mg/kg)、高(8mg/kg)给药组.治疗组于13周开始灌胃荜茇-13味.药物干预8周末结束实验,测定体重、肝湿重和肝指数,检测血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-c)高密度脂蛋白胆固醇(HDL-c)、丙氨酸转移酶(ALT)、门冬氨酸转移酶(AST)、丙二醛(MDA)、超氧化物歧化酶(SOD)和肝组织TG、TC.结果:与对照组比较,模型组体重、肝湿重、肝指数以及血清中TG、TC、LDL-c、、ALT、AST、MDA和肝组织TG、TC含量均增加,具有显著性差异(P〈0.05,P〈0.01)而HDL-c和SOD下降(P〈0.05);与模型组比较,药物干预组大鼠肝湿重和肝指数及血清TG、TC、LDL-c、ALT、AST、MDA和肝组织TG、TC降低,且肝脏脂肪变性和炎症坏死减轻(P〈0.05,P〈0.01).结论:荜茇-13味对大鼠高脂饮食诱导的NAFLD有治疗作用.  相似文献   

3.
将雄性SD大鼠30只随机分三组,其中正常对照组10只,20只通过高脂饲料喂养建立高脂血症大鼠模型后随机分为高脂模型组和高脂运动组.喂养6周后,测定总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、一氧化氮(NO)、一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)、丙二醛(MDA)等相关指标,并进行比较分析.结果显示:对于患高脂血症的大鼠,运动有明显调节血脂、降低过氧化物以及改善血管内皮功能的作用.  相似文献   

4.
目的:观察姜黄素对胰岛素抵抗(IR)大鼠糖脂代谢及血清脂肪细胞因子的影响,探讨姜黄素干预IR的作用机制。方法:采用高脂饲料喂养,建立IR大鼠模型。将IR大鼠随机分为3组:模型组、吡咯列酮组和姜黄素组。给药4周后测定空腹血糖、胰岛素、血脂、TN F-α、Leptin等指标。结果:模型组大鼠血清FIN S、TC、TG和LDL水平均较空白组显著升高,而ISI及HDL水平显著下降;血清TN F-α、Leptin及FFA水平也较空白组明显升高;用姜黄素干预后,大鼠ISI较模型组显著升高,血脂得到改善,FINS、TNF-α、Leptin及FFA水平均显著下降。结论:姜黄素可改善IR大鼠糖脂代谢紊乱,增加胰岛素的敏感性,其机制可能与其调节脂肪细胞因子TNF-α、Leptin的分泌有关。  相似文献   

5.
阿魏酸钠对高脂饮食致动脉粥样硬化的作用   总被引:2,自引:0,他引:2  
目的:探讨阿魏酸钠(SF)抗动脉粥样硬化(AS)的作用及其机理.方法:18只家兔随机分为三组:对照组、高脂组、SF组.分别给予普通饲料、高脂饲料、高脂饲料加SF.10周末颈动脉放血取血样后,处死动物,检查血脂、观察主动脉粥样硬化斑块变化、主动脉超微结构.结果:⑴高脂组和SF组血脂含量显著高于对照组,SF组甘油三脂(TG)含量显著低于高脂组(P<0.05);⑵SF组AS斑块显著低于高脂组(P<0.01);⑶电镜结果显示SF组主动脉损伤明显减轻.结论:SF具有明显的抗AS形成的作用,其机制是:降低血中TG含量,保护内皮细胞.  相似文献   

6.
采用高脂饲料喂养雄性SD大鼠60天,诱导IR及T2DM,并将之随机分为模型组、姜黄素组(80 mg/kg/day)、罗格列酮组(1 mg/kg/day)和两药联用组,在高脂饲料喂养同时给予以上药物。经60天给药后,分别测定各实验组空腹血糖、血浆胰岛素、总胆固醇、高密度脂蛋白、甘油三酯、低密度脂蛋白及游离脂肪酸;稳态模式评估法测定胰岛素抵抗指数;放射免疫法测定TNF-α。结果显示姜黄素能降低高脂饲养大鼠的血糖和提高其胰岛素敏感性,其机制至少部分是由姜黄素显著降低TNF-α水平的抗炎特性及降低血浆游离脂肪酸的抗脂解作用介导。  相似文献   

7.
目的 通过6周运动和魔芋多糖干预,研究其对2型糖尿病大鼠的血糖、胰岛素水平、血脂、肝功能酶、抗氧化指标的影响.方法 本实验将大鼠分为5组:正常对照组(A组),2型糖尿病对照组(B组),2型糖尿病运动组(C组),2型糖尿病魔芋多糖组(D组),2型糖尿病联合强度运动组(E组);每组各10只.测试指标包括:(1)大鼠腹主动脉取血测试空腹血糖、胰岛素水平、TG、TC、HDL-c、LDL-c、ALT、AST;(2)肝组织中SOD和MDA含量.结果 (1)6周运动和魔芋多糖干预明显改善2型糖尿病大鼠血糖和血脂指标,联合干预较单一因素干预效果更加显著(P<0.05);(2)6周运动和魔芋多糖干预均有效降低血清ALT (P<0.01)含量,AST各组均降低(P<0.05);(3)6周运动和魔芋多糖干预有效升高SOD水平、降低MDA水平,联合干预组抗氧化效果更好(P<0.01).结论 通过6周运动和魔芋多糖单独或联合的干预方式,血糖、胰岛素水平和血指标表明:通过干预明显改善2型糖尿病糖、脂代谢紊乱,减少了脂质沉积,降低了转氨酶含量,提高了大鼠抗氧化功能.  相似文献   

8.
目的:选择理想的大鼠高脂血症动物模型造模方法。方法:选取七种大鼠高脂血症动物模型配方,并将其制成乳剂或高脂饲料,取血测定血清中TC、LDL、HDL、TG的含量。结果:其中六种高脂配方均不同程度的使大鼠血清中脂代谢紊乱,形成高血脂动物模型。结论:在猪油和胆固醇的基础上同时加入胆盐和丙基硫氧嘧啶可以形成理想的大鼠高脂血症动物模型。  相似文献   

9.
目的:探讨金边瑞香活性成分瑞香素对家兔实验性动脉粥样硬化的影响及其作用机制。方法:18只家兔随机分为3组,即正常对照组(6只)、高脂模型对照组(6只)、瑞香素药物组(6只);正常对照组饲普通标准饲料,模型对照组、瑞香素药物组先导管球囊损伤兔左侧颈总动脉然后喂饲高脂饲料;同时瑞香素药物组每天灌胃瑞香素液800mg/kg,而正常对照组、模型对照组灌胃等量生理水。实验满90天后停药禁食12h,耳缘静脉取血9~10mL用于做血脂、Hs-CRP检查;用10%乌拉坦耳缘静脉注射麻醉,分离左侧颈总动脉,用免疫组织化学法测定组织Hs-CRP含量,在显微镜下观察颈动脉内膜斑块的病理学改变。结果:正常对照组与模型对照组血脂,血清及斑块组织Hs-CRP水平有显著性差异(P〈0.01),瑞香素药物组与模型对照组血脂、血清及斑块组织Hs-CRP水平有显著性差异(P〈0.01)。结论:金边瑞香活性成分瑞香素有抗动脉粥样硬化的作用,其作用机制可能为调脂,抗炎症反应。  相似文献   

10.
目的:探讨芦丁对高脂饮食引起的小鼠心肌损伤的保护作用.方法:24只ICR小鼠随机分为如下3组:正常对照组(CTRL组)喂养普通饲料,高脂饮食组(HFD组)喂养高脂饲料,芦丁干预高脂饮食组(RHFD组)喂养高脂饲料+芦丁干预.每周称重1次,观察行为,喂养15周后,收集血液样本,处死小鼠.采集心脏组织,HE染色进行分析心肌组织形态学,观察其病理变化.检测血清丙谷转氨酶(GPT)、乳酸脱氢酶(LDH)的活性以及总胆固醇(TC)和甘油三酯(TG)含量.结果:饲喂15周后,与HFD组比较,CTRL组和RHFD组体重增长缓慢;与CTRL组相比,HFD组GPT、LDH活性和TC、TG含量均显著升高(P<0.05);与HFD组比较,RHFD组的GPT、LDH活性和TC、TG含量降低,尤其是LDH活性和TG含量减少明显(P<0.05).心肌组织HE染色显示HFD组心肌纤维发生断裂现象,心肌间质增宽,排列紊乱,可见少量心肌细胞变形、坏死,局部产生炎细胞浸润,产生肌浆溶解和空泡样病变,出现炎性浸润水肿.RHFD组可见心肌细胞排列非常整齐,心肌纤维无明显增粗肥大,无明显水肿,较高脂饮食组有明显改善.结论:芦丁对高脂饮食造成的肥胖引起的心肌损伤有良好的保护作用.  相似文献   

11.
Objective: The prevalence of non-alcoholic fatty liver disease (NAFLD) has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone (PGZ) acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. Methods: The rats were separated randomly into 6 groups: model group Ⅰ were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/(kg.d) simultaneously, while control group Ⅰ were fed normal food for 8 weeks; model group Ⅱ were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/(kg.d) orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group Ⅱ were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), tumor necrosis factor alpha (TNF-α), fasting blood glucose (FBG), fasting plasma insulin (FINS), HOMA (homeostasis model assessment) insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed. Results: After 8 weeks, the liver in model group Ⅰ showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-α were significantly increased (P〈0.05) compared with control group Ⅰ. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased (P〈0.05) compared with model group Ⅰ. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group Ⅱ rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels ofALT, AST, ALP, FINS and HOMA-IR were significantly increased (P〈0.05) in model group Ⅱ compared with control group Ⅱ. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-α and HOMA-IR were significantly decreased compared with model group Ⅱ. Conclusion: Insulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.  相似文献   

12.
Objectives:To investigate the intestinal microflora status related to ischemia/reperfusion(I/R)liver injury and explorethe possible mechanism.Methods:Specific pathogen free grade Sprague-Dawley rats were randomized into three groups:Controlgroup(n=8),sham group(n=6)and I/R group(n=10).Rats in the control group did not receive any treatment,rats in the I/R groupwere subjected to 20 min of liver ischemia,and rats in the sham group were only subjected to sham operation.Twenty-two hourslater,the rats were sacrificed and liver enzymes and malondialdehyde(MDA),superoxide dismutase(SOD),serum endotoxin,intestinal bacterial counts,intestinal mucosal histology,bacterial translocation to mesenteric lymph nodes,liver,spleen,andkidney were studied.Results:Ischemia/reperfusion increased liver enzymes,MDA,decreased SOD,and was associated withplasma endotoxin elevation in the I/R group campared to those in the sham group.Intestinal Bifidobacteria and Lactobacillidecreased and intestinal Enterobacterium and Enterococcus  相似文献   

13.
Because of their physiological similarity to humans, pigs provide an excellent model for the study of obesity. This study evaluated diet-induced adiposity in genetically lean pigs and found that body weight and energy intake did not differ between controls and pigs fed the high-fat (HF) diet for three months. However, fat mass percentage, adipocyte size, concentrations of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), insulin, and leptin in plasma were significantly higher in HF pigs than in controls. The HF diet increased the expression in backfat tissue of genes responsible for cholesterol synthesis such as Insig-1 and Insig-2. Lipid metabolism-related genes including sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthase 1 (FASN1), diacylglycerol O-acyltransferase 2 (DGAT2), and fatty acid binding protein 4 (FABP4) were significantly up-regulated in backfat tissue, while the expression of proliferator-activated receptor-α (PPAR-α) and carnitine palmitoyl transferase 2 (CPT2), both involved in fatty acid oxidation, was reduced. In liver tissue, HF feeding significantly elevated the expression of SREBP-1c, FASN1, DGAT2, and hepatocyte nuclear factor-4α (HNF-4α) mRNAs. Microarray analysis further showed that the HF diet had a significant effect on the expression of 576 genes. Among these, 108 genes were related to 21 pathways, with 20 genes involved in adiposity deposition and 26 related to immune response. Our results suggest that an HF diet can induce genetically lean pigs into obesity with body fat mass expansion and adipose-related inflammation.  相似文献   

14.
目的:观察黄芩甙注射液对四氯化碳(CCl4)致急性肝损伤小鼠肝抗氧化功能的影响。方法:50只小鼠随机分为5组,每组10只,分别为对照组、模型组、黄芩甙注射液低、中、高(0.25 g/kg、0.50 g/kg、1.00g/kg)剂量组。用CCl4制备小鼠急性肝损伤模型,测定小鼠体重变化,肝指数,肝超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性,谷胱甘肽(GSH)及丙二醛(MDA)含量。结果:与对照组及模型组比较,黄芩甙各剂量组小鼠试验前后的体重及肝指数差异不显著(P>0.05)。与模型组比较,低剂量组小鼠肝SOD、GSH-Px活性及MDA含量差异不显著(P>0.05),而GSH含量显著升高(P<0.05);中、高剂量组SOD、GSH-Px活性极显著提高(P<0.01),GSH含量极显著升高(P<0.01),MDA含量极显著降低(P<0.01)。结论:黄芩甙能显著增强急性肝损伤小鼠肝SOD、GSH-Px活性,提高GSH含量,降低MDA含量,并表现正向的量效关系。  相似文献   

15.
目的:探讨辛伐他汀治疗脂肪肝的的临床疗效。方法:120例脂肪肝患者随机分为两组,辛伐他汀治疗组60例采用辛伐他汀20mg,每天1次口服;血脂康治疗组60例采用血脂康600mg,每天2次口服。8周为1个疗程,共3个疗程,观察辛伐他汀治疗组与血脂康治疗组的临床疗效、治疗前后血脂和B超变化情况,另选择同期体检证明为正常的健康者70人作为对照组。结果:辛伐他汀治疗组总有效率(93.1%)与血脂康组(90.3%)相似(P>0.05);辛伐他汀治疗组和血脂康治疗组治疗后与治疗前相比血总胆固醇(TC)、甘油三脂(TG)、高密度脂蛋白(HDL-C)均明显改善(P<0.01),辛伐他汀治疗组改善优于血脂康组(P<0.05或P<0.01),辛伐他汀治疗组与血脂康治疗组两组治疗后肝功能与治疗前相比均明显改善(P<0.01),但辛伐他汀治疗组与血脂康治疗组两组治疗后相比无显著差异(P>0.05),未见严重不良反应。结论:辛伐他汀是治疗高血脂和脂肪肝的有效药物之一,且副作用少,安全性大,值得临床应用。  相似文献   

16.
目的探讨丹参注射液抗肝纤维化作用机理.方法取40只成年wistar大鼠,利用猪血清腹腔注射法,连续6周,复制免疫性肝纤维化模型.治疗组采用大、小剂量丹参液肌肉注射,其剂量分别为0.3ml/kg和0.15ml/kg,每日一次,连续4周.取肝脏切片,HE和Mollory染色,光镜下观察.检测血清SOD活性、MDA含量和肝功能.结果大剂量治疗组肝细胞空泡减少,胶原纤维大部分消失,SOD活性增高,MDA含量降低,与模型组比较有显著性差异(P<0.05).结论大剂量肌注丹参液,具有治疗肝纤维化的功能.  相似文献   

17.
目的:评价超声测量内脏脂肪厚度对非酒精性脂肪性肝病(NAFLD)的诊断和分级的价值。方法:收集2010年8月至2011年4月在某院体检中心进行健康体检资料共122例,NAFLD组74例,非NAFLD组48例,经超声测量内脏脂肪厚度。结果:超声测量内脏脂肪厚度在NAFLD组和非NAFLD组之间差异有显著性统计学意义(P=0.004)。轻度、中度、重度NAFLD组测量的内脏脂肪厚度经方差分析结果为差异有统计学意义(F=9.91,P〈0.001),进一步用LSD法分析显示两两之间都有差异。经超声测量的VFT诊断NAFLD的ROC曲线下面积为0.794,p=0.011,诊断切点值为2.70cm。结论:经超声测量的内脏脂肪厚度可作为NAFLD诊断和分级的指标。  相似文献   

18.
目的::观察三叶悬钩子乙醇提取物对大鼠酒精性肝炎的保护作用。方法:90只大鼠,随机分为6组,每天上午8:00灌胃1次,正常组大鼠灌胃给蒸馏水,其余5组大鼠灌胃给白酒,连续灌胃28 d,建立大鼠酒精性肝炎模型;第15天开始,每天上午9:00各组大鼠均以相应药物灌胃1次,连续灌胃14 d;第28天末次灌胃后,取血、取肝脏,检测血清天门冬氨酸氨基转移酶(GOT)、丙氨酸氨基转移酶(GPT)活性及肝组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性;观察肝脏指数及肝组织病理变化。结果:三叶悬钩子乙醇提取物能显著降低肝炎大鼠GPT、GOT活性和MDA含量,能显著提高肝炎大鼠SOD活性;能显著降低肝炎大鼠肝脏指数;能显著减轻肝炎大鼠肝组织水肿和脂肪变性。结论:三叶悬钩子对大鼠酒精性肝炎有保护作用。  相似文献   

19.
To investigate the effects of hypoxic exercise training on microRNA (miRNA) expression and the role of miRNA expression in regulating lipid metabolism, 20 dietary-induced obese SD rats were divided into a normoxic sedentary group (N, n=10) and a hypoxic exercise training group (H, n=10). After four weeks, measurements were taken of body weight, body length, fat mass, serum lipid concentration, miRNAs differentially expressed in rat liver, and gene and protein expression levels of peroxisome proliferator activated receptor α (PPARα), fatty acid synthetase (FAS), and carnitine palmitoyl transferase 1A (CPT1A) in rat liver. Body weight, Lee’s index, fat mass, fat/weight ratio, and serum levels of total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) were all significantly lower in the H group than in the N group (P<0.01). Six miRNAs expressed significantly differently in the liver (P<0.05). Specifically, expression levels of miR-378b were significantly lower in the H group than in the N group (P<0.05). Compared with the normoxic sedentary group, hypoxic exercise training resulted in a lower ratio of FAS mRNA to CPT1A mRNA (P<0.05), as well as lower CPT1A protein levels (P<0.01), while a higher ratio of FAS to CPT1A protein levels (P<0.01) was observed. In conclusion, hypoxic training may elevate the resistance of high fat diet induced obesity in rats by reducing the expression of miR-378b, and decrease the fatty acid mitochondrial oxidation in obese rat livers by decreasing the protein expression of CPT1A and increasing the protein expression ratio of FAS/CPT1A.  相似文献   

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