Scavenger receptor class B type Ⅰ (SR-BI) is an important member of the scavenger receptor family of integral membrane glycoproteins. This review highlights studies in SR-BI knockout mice, which concern the role of S...Scavenger receptor class B type Ⅰ (SR-BI) is an important member of the scavenger receptor family of integral membrane glycoproteins. This review highlights studies in SR-BI knockout mice, which concern the role of SR-BI in cholesterol and steroid metabolism. SR-BI in hepatocytes is the sole molecule involved in selective uptake of cholesteryl esters from high-density lipoprotein (HDL). SR-BI plays a physiological role in binding and uptake of native apolipoprotein B (apoB)-containing lipoproteins by hepatocytes, which identif ies SR-BI as a multipurpose player in lipid uptake from the blood circulation into hepatocytes in mice. In adrenocortical cells, SR-BI mediates the selective uptake of HDL-cholesteryl esters, which is eff iciently coupled to the synthesis of glucocorticoids (i.e. corticosterone). SR-BI knockout mice suffer from adrenal glucocorticoid insuff iciency, which suggests that functional SR-BI protein is necessary for optimal adrenal steroidogenesis in mice. SR-BI in macrophages plays a dual role in cholesterol metabolism as it is able to take up cholesterol associated with HDL and apoBcontaining lipoproteins and can possibly facilitate cholesterol efflux to HDL. Absence of SR-BI is associated with thrombocytopenia and altered thrombosis susceptibility, which suggests a novel role for SR-BI in regulating platelet number and function in mice. Transgenic expression of cholesteryl ester transfer protein in humanized SR-BI knockout mice normalizes hepatic delivery of HDL-cholesteryl esters. However, other pathologies associated with SR-BI def iciency, i.e. increased atherosclerosis susceptibility, adrenal glucocorticoid insuffi ciency, and impaired platelet function are not normalized, which suggests an important role for SR-BI in cholesterol and steroid metabolism in man. In conclusion, generation of SR-BI knockout mice has signif icantly contributed to our knowledge of the physiological role of SR-BI. Studies using these mice have identif ied SR-BI as a multi-purpose player in cholesterol and stero展开更多
目的:研究小檗碱(Berberine,Ber)对高脂兔模型脂代谢和血管硬化的影响,并探讨其可能的作用机制。方法:采用高脂饲料喂养2月建立高脂兔动物模型。40只新西兰大耳白兔随机分成普通饲料组(普食组)、高脂模型组、高脂+Ber组[28、112mg/(kg....目的:研究小檗碱(Berberine,Ber)对高脂兔模型脂代谢和血管硬化的影响,并探讨其可能的作用机制。方法:采用高脂饲料喂养2月建立高脂兔动物模型。40只新西兰大耳白兔随机分成普通饲料组(普食组)、高脂模型组、高脂+Ber组[28、112mg/(kg.d)]、高脂+非诺贝特组[30 mg/(kg.d)]。2月后测定各组血清总胆固醇(Total cholesterol,TC)、三酰基甘油(Triglycerides,TG)、低密度脂蛋白胆固醇(Low density lipoprotein-cholesterol,LDL-C)、高密度脂蛋白胆固醇(High density lipoprotein-choles-terol,HDL-C)水平;HE染色观察主动脉组织形态学变化;实时荧光定量PCR检测主动脉诱导型一氧化氮合酶(Inductible nitricoxide synthase,iNOS)和B类1型清道夫受体(Scavenger receptor class-B type 1,SR-B1)基因表达的变化。结果:与普食组相比,高脂模型组TC、TG和LDL-C水平显著升高(P<0.05),主动脉内膜出现明显的脂质沉积和泡沫细胞形成,iNOS和SR-B1 mR-NA表达显著升高(P<0.05);与高脂模型组相比,高脂+Ber处理组血清TC、TG和LDL-C的水平显著降低(P<0.05),而HDL水平显著升高(P<0.05),主动脉粥内膜脂质沉积减轻,泡沫细胞明显减少,iNOS和SR-B1 mRNA表达显著降低(P<0.05)。结论:Ber具有明显的调血脂和抗血管硬化作用,其作用机制与抑制iNOS和SR-B1基因表达相关。展开更多
Biliary cholesterol secretion is a process important for 2 major disease complexes, atherosclerotic cardiovascular disease and cholesterol gallstone disease. With respect to cardiovascular disease, biliary cholesterol...Biliary cholesterol secretion is a process important for 2 major disease complexes, atherosclerotic cardiovascular disease and cholesterol gallstone disease. With respect to cardiovascular disease, biliary cholesterol secretion is regarded as the f inal step for the elimination of cholesterol originating from cholesterol-laden macrophage foam cells in the vessel wall in a pathway named reverse cholesterol transport. On the other hand, cholesterol hypersecretion into the bile is considered the main pathophysiological determinant of cholesterol gallstone formation. This review summarizes current knowledge on the origins of cholesterol secreted into the bile as well as the relevant processes and transporters involved. Next to the established ATP-binding cassette (ABC) transporters mediating the biliary secretion of bile acids (ABCB11), phospholipids (ABCB4) and cholesterol (ABCG5/G8), special attention is given to emerging proteins that modulate or mediate biliary cholesterol secretion. In this regard, the potential impact of the phosphatidylserine flippase ATPase class Ⅰ type 8B member 1, the Niemann Pick C1-like protein 1 that mediatescholesterol absorption and the high density lipoprotein cholesterol uptake receptor, scavenger receptor class B type Ⅰ, is discussed.展开更多
为探讨血清淀粉样蛋白A(serum amyloid A,SAA)对巨噬细胞B类I型清道夫受体(scavenger receptor class B type I,SR-BI)的表达以及炎症反应的影响及分子机制,采用SAA、p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38-M...为探讨血清淀粉样蛋白A(serum amyloid A,SAA)对巨噬细胞B类I型清道夫受体(scavenger receptor class B type I,SR-BI)的表达以及炎症反应的影响及分子机制,采用SAA、p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38-MAPK)激动剂anisomycin或抑制剂SB203580处理THP-1巨噬细胞,以实时定量PCR、Western blot和ELISA分别检测细胞中SR-BI、炎症因子及磷酸化p38-MAPK的表达。结果显示,与对照组相比,SAA处理THP-1细胞后,SR-BI的表达下调,而炎症因子与磷酸化p38蛋白的表达则上调,且这种效应呈浓度和时间依赖性(P<0.05)。与SAA单独处理组比较,SAA与p38-MAPK激动剂anisomycin共孵育细胞后,细胞SR-BI表达下调,炎症因子及磷酸化p38蛋白表达增加(P<0.05);而SAA与p38-MAPK抑制剂SB203580共同处理细胞后,细胞SR-BI表达增加,炎症因子及磷酸化p38蛋白表达减少(P<0.05)。结果提示,SAA可促进THP-1巨噬细胞炎症反应,其机制与p38-MAPK的磷酸化及SR-BI表达的下调有关。展开更多
Atherosclerosis is a leading underlying factor in cardiovascular disease and stroke,important causes of morbidity and mortality across the globe.Abundant epidemiological studies demonstrate that high levels of high de...Atherosclerosis is a leading underlying factor in cardiovascular disease and stroke,important causes of morbidity and mortality across the globe.Abundant epidemiological studies demonstrate that high levels of high density lipoprotein（HDL） are associated with reduced risk of atherosclerosis and preclinical,animal model studies demonstrate that this association is causative.Understanding the molecular mechanisms underlying the protective effects of HDL will allow more strategic approaches to development of HDL based therapeutics.Recent evidence suggests that an important aspect of the ability of HDL to protect against atherosclerosis is its ability to trigger signaling responses in a variety of target cells including endothelial cells and macrophages in the vessel wall.These signaling responses require the HDL receptor,scavenger receptor class B type 1（SR-B1）,an adaptor protein（PDZK1） that binds to the cytosolic C terminus of SR-B1,Akt1 activation and（at least in endothelial cells） activation of endothelial NO synthase（eNOS）.Mouse models of atherosclerosis,exemplified by apolipoprotein E or low density lipoprotein receptor gene inactivated mice（apoE or LDLR KO） develop atherosclerosis in their aortas but appear generally resistant to coronary artery atherosclerosis.On the other hand,inactivation of each of the components of HDL signaling（above）in either apoE or LDLR KO mice renders them susceptible to extensive coronary artery atherosclerosis suggesting that HDL signaling may play an important role in protection against coronary artery disease.展开更多
BACKGROUND:Non-alcoholic fatty liver disease(NAFLD)is one of the most frequent causes of liver diseases,with markedly increased prevalence.However,its mechanisms are not clear.The present study was undertaken to illus...BACKGROUND:Non-alcoholic fatty liver disease(NAFLD)is one of the most frequent causes of liver diseases,with markedly increased prevalence.However,its mechanisms are not clear.The present study was undertaken to illustrate the role of caveolin-1(cav1)and the scavenger receptor class B type 1(SR-B1)in NAFLD.METHODS:Adult male C57BL/6 mice were fed with a normal diet or high fat and cholesterol(HFC)diet for 14 weeks.The mice were sacrificed to collect plasma and harvest the liver;their plasma lipid concentration was measured.Hepatic cav1and SR-B1 mRNA and protein expression were determined by real-time quantitative polymerase chain reaction(qPCR)and Western blotting,respectively.In order to study cav1 and SR-B1distribution and change in hepatocytes,immunohistochemical analysis was performed.RESULTS:HFC diet increased plasma lipids,induced NAFLD and increased the liver/body weight ratio.Compared to the control mice(n=6),the mRNA and protein levels of cav1 and SR-B1 in liver tissue of the NAFLD mice(n=12)increased significantly(cav1 mRNA:1.536±0.226 vs 0.980±0.272,P【0.05;protein:0.643±0.240 vs 0.100±0.130,P【0.01;SR-B1 mRNA:1.377±0.125 vs 0.956±0.151,P【0.01;protein:2.156±0.507vs 0.211±0.211,P【0.01).Furthermore,both cav1 and SR-B1immunoreactivity increased and their distribution was also changed,mainly in the plasma membrane of hepatocytes,cytoplasm and membrane of lipid droplets and around.CONCLUSION:NAFLD is associated with increased concentration of plasma lipids and upregulation of hepatic cav1 and SR-B1 gene and protein expressions,which indicate that cav1 and SR-B1 might play crucial roles in the pathogenesis of NAFLD.展开更多
目的:探讨电针丰隆穴对高脂血症大鼠血脂水平、肝脏组织的清道夫受体BI(scavenger receptor clas s B type I,SR-BI)、过氧化物酶体增殖物激活型受体γ(peroxi some proliferator-activated receptor-γPPARγ)的mRNA相对表达量及腹腔...目的:探讨电针丰隆穴对高脂血症大鼠血脂水平、肝脏组织的清道夫受体BI(scavenger receptor clas s B type I,SR-BI)、过氧化物酶体增殖物激活型受体γ(peroxi some proliferator-activated receptor-γPPARγ)的mRNA相对表达量及腹腔巨噬细胞炎症相关因子细胞间黏附因子-1(intercellular adhesion molecule-1,ICAM-1)、白介素-1β(intefleukin-1β,IL-1β)、IL-10含量的影响及其相关作用机制.方法:将SD大鼠随机分为空白对照组、模型对照组、电针1组、电针2组这4组,每组10只.治疗结束后检测各组血脂含量,肝脏组织中SR-BI、PPARγ的mRNA相对表达量.最后分离出大鼠腹腔中的巨噬细胞,应用流式细胞仪检测炎症相关因子ICAM-1、IL-1β、IL-10的含量.结果:与空白对照组比较,模型对照组TG.变化并不明显(p>0.05),而总胆固醇(total chole sterol,TC)、低密度脂蛋白-胆固醇(loW density lipoprotein cholesterol,LDL-C)明显上升(P<0.01),高密度脂蛋白-胆固醇(high density lipoprotein cholesterol,HDL-C).明显下降(P<0.01);与模型对照组比较,电.针l组及电针2组的TG和HDL-C变化并不明显(P>0.05),大鼠血清TC、LDL-C均有显著下降(P<0.01);与电针1组比较,电针2组TC、LDL-C均有降低(P<0.01,P<0.05).与空白对照组比较,除了电针2组外,其余两组SR-BI、PPAR7均有显著降低(P<0.05,P<0.01);与模型对照组比较,电针1组和电针2组的SR-BI、PPARγ均有显著升高(P<0.05,P<0.01),其中电针2组更为显著(P<0.01).与空白对照组比较,除电针2组外,模型对照组和电针1组的炎症因子ICAM-1、IL-1β均有显著性升高(P<0.05,P<0.01),而模型对照组的抗炎因子IL-10有显著下降(P<0.01);与模型对照组比较,电针1组和电针2组的炎症因子ICAM-1、IL-1β均有非常显著性减少(P<0.01),而抗炎因子IL-10的含量有非常显著性升高(p<0.01).结论:通过电针丰隆穴治疗能降低高脂血症模型大鼠的TC、LDL-C水平,升高HDL-C水平,增加肝脏SR-BI、PPARγmRNA相对表�展开更多
基金Supported by Top Institute Pharma (TIPharma Project T2-110 Hoekstra M and Van Berkel TJC)+2 种基金Grant 2008T070 from the Netherlands Heart Foundation (Hoekstra M)VIDI Grant 917.66.301 from the Netherlands Organization for Scientific Research (Van Eck M)Van Eck Mis an Established Investigator of the Netherlands Heart Foundation (Grant 2007T056)
文摘Scavenger receptor class B type Ⅰ (SR-BI) is an important member of the scavenger receptor family of integral membrane glycoproteins. This review highlights studies in SR-BI knockout mice, which concern the role of SR-BI in cholesterol and steroid metabolism. SR-BI in hepatocytes is the sole molecule involved in selective uptake of cholesteryl esters from high-density lipoprotein (HDL). SR-BI plays a physiological role in binding and uptake of native apolipoprotein B (apoB)-containing lipoproteins by hepatocytes, which identif ies SR-BI as a multipurpose player in lipid uptake from the blood circulation into hepatocytes in mice. In adrenocortical cells, SR-BI mediates the selective uptake of HDL-cholesteryl esters, which is eff iciently coupled to the synthesis of glucocorticoids (i.e. corticosterone). SR-BI knockout mice suffer from adrenal glucocorticoid insuff iciency, which suggests that functional SR-BI protein is necessary for optimal adrenal steroidogenesis in mice. SR-BI in macrophages plays a dual role in cholesterol metabolism as it is able to take up cholesterol associated with HDL and apoBcontaining lipoproteins and can possibly facilitate cholesterol efflux to HDL. Absence of SR-BI is associated with thrombocytopenia and altered thrombosis susceptibility, which suggests a novel role for SR-BI in regulating platelet number and function in mice. Transgenic expression of cholesteryl ester transfer protein in humanized SR-BI knockout mice normalizes hepatic delivery of HDL-cholesteryl esters. However, other pathologies associated with SR-BI def iciency, i.e. increased atherosclerosis susceptibility, adrenal glucocorticoid insuffi ciency, and impaired platelet function are not normalized, which suggests an important role for SR-BI in cholesterol and steroid metabolism in man. In conclusion, generation of SR-BI knockout mice has signif icantly contributed to our knowledge of the physiological role of SR-BI. Studies using these mice have identif ied SR-BI as a multi-purpose player in cholesterol and stero
文摘目的:研究小檗碱(Berberine,Ber)对高脂兔模型脂代谢和血管硬化的影响,并探讨其可能的作用机制。方法:采用高脂饲料喂养2月建立高脂兔动物模型。40只新西兰大耳白兔随机分成普通饲料组(普食组)、高脂模型组、高脂+Ber组[28、112mg/(kg.d)]、高脂+非诺贝特组[30 mg/(kg.d)]。2月后测定各组血清总胆固醇(Total cholesterol,TC)、三酰基甘油(Triglycerides,TG)、低密度脂蛋白胆固醇(Low density lipoprotein-cholesterol,LDL-C)、高密度脂蛋白胆固醇(High density lipoprotein-choles-terol,HDL-C)水平;HE染色观察主动脉组织形态学变化;实时荧光定量PCR检测主动脉诱导型一氧化氮合酶(Inductible nitricoxide synthase,iNOS)和B类1型清道夫受体(Scavenger receptor class-B type 1,SR-B1)基因表达的变化。结果:与普食组相比,高脂模型组TC、TG和LDL-C水平显著升高(P<0.05),主动脉内膜出现明显的脂质沉积和泡沫细胞形成,iNOS和SR-B1 mR-NA表达显著升高(P<0.05);与高脂模型组相比,高脂+Ber处理组血清TC、TG和LDL-C的水平显著降低(P<0.05),而HDL水平显著升高(P<0.05),主动脉粥内膜脂质沉积减轻,泡沫细胞明显减少,iNOS和SR-B1 mRNA表达显著降低(P<0.05)。结论:Ber具有明显的调血脂和抗血管硬化作用,其作用机制与抑制iNOS和SR-B1基因表达相关。
基金Supported by A grant from the Netherlands Organization for Scientif ic Research (NWO, VIDI Grant 917-56-358)
文摘Biliary cholesterol secretion is a process important for 2 major disease complexes, atherosclerotic cardiovascular disease and cholesterol gallstone disease. With respect to cardiovascular disease, biliary cholesterol secretion is regarded as the f inal step for the elimination of cholesterol originating from cholesterol-laden macrophage foam cells in the vessel wall in a pathway named reverse cholesterol transport. On the other hand, cholesterol hypersecretion into the bile is considered the main pathophysiological determinant of cholesterol gallstone formation. This review summarizes current knowledge on the origins of cholesterol secreted into the bile as well as the relevant processes and transporters involved. Next to the established ATP-binding cassette (ABC) transporters mediating the biliary secretion of bile acids (ABCB11), phospholipids (ABCB4) and cholesterol (ABCG5/G8), special attention is given to emerging proteins that modulate or mediate biliary cholesterol secretion. In this regard, the potential impact of the phosphatidylserine flippase ATPase class Ⅰ type 8B member 1, the Niemann Pick C1-like protein 1 that mediatescholesterol absorption and the high density lipoprotein cholesterol uptake receptor, scavenger receptor class B type Ⅰ, is discussed.
基金supported by grants from the National Natural Science Foundation of China(No.81100211)the Natural Science Foundation of Hunan Province+7 种基金China(No.14JJ208414JJ5016)the Science and Technology Project of Hengyang CityHunan ProvinceChina(No.2013KJ04)the Construct Program of the Key Discipline in Hunan ProvinceChina(Basic Medicine Sciences in University of South China)Zhengxiang Scholar Program of the University of South China
文摘为探讨血清淀粉样蛋白A(serum amyloid A,SAA)对巨噬细胞B类I型清道夫受体(scavenger receptor class B type I,SR-BI)的表达以及炎症反应的影响及分子机制,采用SAA、p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38-MAPK)激动剂anisomycin或抑制剂SB203580处理THP-1巨噬细胞,以实时定量PCR、Western blot和ELISA分别检测细胞中SR-BI、炎症因子及磷酸化p38-MAPK的表达。结果显示,与对照组相比,SAA处理THP-1细胞后,SR-BI的表达下调,而炎症因子与磷酸化p38蛋白的表达则上调,且这种效应呈浓度和时间依赖性(P<0.05)。与SAA单独处理组比较,SAA与p38-MAPK激动剂anisomycin共孵育细胞后,细胞SR-BI表达下调,炎症因子及磷酸化p38蛋白表达增加(P<0.05);而SAA与p38-MAPK抑制剂SB203580共同处理细胞后,细胞SR-BI表达增加,炎症因子及磷酸化p38蛋白表达减少(P<0.05)。结果提示,SAA可促进THP-1巨噬细胞炎症反应,其机制与p38-MAPK的磷酸化及SR-BI表达的下调有关。
基金supported by funds from the Canadian Institutes of Health Research (MOP74765)the Heart and Stroke Foundation of Canada(G-13-0002833 and G-15-0009016)
文摘Atherosclerosis is a leading underlying factor in cardiovascular disease and stroke,important causes of morbidity and mortality across the globe.Abundant epidemiological studies demonstrate that high levels of high density lipoprotein（HDL） are associated with reduced risk of atherosclerosis and preclinical,animal model studies demonstrate that this association is causative.Understanding the molecular mechanisms underlying the protective effects of HDL will allow more strategic approaches to development of HDL based therapeutics.Recent evidence suggests that an important aspect of the ability of HDL to protect against atherosclerosis is its ability to trigger signaling responses in a variety of target cells including endothelial cells and macrophages in the vessel wall.These signaling responses require the HDL receptor,scavenger receptor class B type 1（SR-B1）,an adaptor protein（PDZK1） that binds to the cytosolic C terminus of SR-B1,Akt1 activation and（at least in endothelial cells） activation of endothelial NO synthase（eNOS）.Mouse models of atherosclerosis,exemplified by apolipoprotein E or low density lipoprotein receptor gene inactivated mice（apoE or LDLR KO） develop atherosclerosis in their aortas but appear generally resistant to coronary artery atherosclerosis.On the other hand,inactivation of each of the components of HDL signaling（above）in either apoE or LDLR KO mice renders them susceptible to extensive coronary artery atherosclerosis suggesting that HDL signaling may play an important role in protection against coronary artery disease.
基金supported by a grant from the National Natural Science Foundation of China(491010-N11026)
文摘BACKGROUND:Non-alcoholic fatty liver disease(NAFLD)is one of the most frequent causes of liver diseases,with markedly increased prevalence.However,its mechanisms are not clear.The present study was undertaken to illustrate the role of caveolin-1(cav1)and the scavenger receptor class B type 1(SR-B1)in NAFLD.METHODS:Adult male C57BL/6 mice were fed with a normal diet or high fat and cholesterol(HFC)diet for 14 weeks.The mice were sacrificed to collect plasma and harvest the liver;their plasma lipid concentration was measured.Hepatic cav1and SR-B1 mRNA and protein expression were determined by real-time quantitative polymerase chain reaction(qPCR)and Western blotting,respectively.In order to study cav1 and SR-B1distribution and change in hepatocytes,immunohistochemical analysis was performed.RESULTS:HFC diet increased plasma lipids,induced NAFLD and increased the liver/body weight ratio.Compared to the control mice(n=6),the mRNA and protein levels of cav1 and SR-B1 in liver tissue of the NAFLD mice(n=12)increased significantly(cav1 mRNA:1.536±0.226 vs 0.980±0.272,P【0.05;protein:0.643±0.240 vs 0.100±0.130,P【0.01;SR-B1 mRNA:1.377±0.125 vs 0.956±0.151,P【0.01;protein:2.156±0.507vs 0.211±0.211,P【0.01).Furthermore,both cav1 and SR-B1immunoreactivity increased and their distribution was also changed,mainly in the plasma membrane of hepatocytes,cytoplasm and membrane of lipid droplets and around.CONCLUSION:NAFLD is associated with increased concentration of plasma lipids and upregulation of hepatic cav1 and SR-B1 gene and protein expressions,which indicate that cav1 and SR-B1 might play crucial roles in the pathogenesis of NAFLD.
文摘目的:观察氧化型低密度脂蛋白(oxidized low-density lipoprotein,ox-LDL)干预是否刺激分化成熟的3T3-L1脂肪细胞胆固醇流出,并探讨其机制。方法:3T3-L1细胞促分化成熟后,给予不同浓度的ox-LDL(0～50μg/mL)干预8或24h;在以25μg/mL ox-LDL预处理脂肪细胞24h后,再以10μmol/L22(R)-羟基胆固醇干预24h,收集细胞,采用逆转录聚合酶链反应(reverse transcription polymer-ase chain reaction,RT-PCR)测定脂肪细胞三磷酸腺苷结合盒转运体A1(ATP binding cassette transporterA1,ABCA1),B族I型清道夫受体(scavenger receptor class B type I,SR-BI)和肝X受体α(liver X receptorα,LXRα)mRNA表达,采用液体闪烁计数器检测载脂蛋白A-I(apolipoprotein A-I,apoA-I)介导的细胞内胆固醇流出。结果:低浓度ox-LDL(12.5～25μg/mL)干预24h可增加脂肪细胞ABCA1,LXRα和SR-BImRNA的表达,并促进apoA-I介导的胆固醇流出,而高浓度(50μg/mL)则无此作用。将脂肪细胞用25μg/mL ox-LDL预处理24h,再用10μmol/L22(R)-羟基胆固醇干预细胞,ABCA1和LXRαmRNA表达均有显著增加(P<0.01),同时apoA-I介导的胆固醇流出增加,而SR-BImRNA表达无明显改变。结论:低浓度ox-LDL不仅可促进脂肪细胞LXRα-ABCA1-apoA-I通路,还可上调SR-BI表达,加速细胞内胆固醇流出。Ox-LDL这种新的作用不仅有利于维持脂肪细胞内胆固醇的动态平衡,还可能具有抗动脉粥样硬化作用。
文摘目的:探讨电针丰隆穴对高脂血症大鼠血脂水平、肝脏组织的清道夫受体BI(scavenger receptor clas s B type I,SR-BI)、过氧化物酶体增殖物激活型受体γ(peroxi some proliferator-activated receptor-γPPARγ)的mRNA相对表达量及腹腔巨噬细胞炎症相关因子细胞间黏附因子-1(intercellular adhesion molecule-1,ICAM-1)、白介素-1β(intefleukin-1β,IL-1β)、IL-10含量的影响及其相关作用机制.方法:将SD大鼠随机分为空白对照组、模型对照组、电针1组、电针2组这4组,每组10只.治疗结束后检测各组血脂含量,肝脏组织中SR-BI、PPARγ的mRNA相对表达量.最后分离出大鼠腹腔中的巨噬细胞,应用流式细胞仪检测炎症相关因子ICAM-1、IL-1β、IL-10的含量.结果:与空白对照组比较,模型对照组TG.变化并不明显(p>0.05),而总胆固醇(total chole sterol,TC)、低密度脂蛋白-胆固醇(loW density lipoprotein cholesterol,LDL-C)明显上升(P<0.01),高密度脂蛋白-胆固醇(high density lipoprotein cholesterol,HDL-C).明显下降(P<0.01);与模型对照组比较,电.针l组及电针2组的TG和HDL-C变化并不明显(P>0.05),大鼠血清TC、LDL-C均有显著下降(P<0.01);与电针1组比较,电针2组TC、LDL-C均有降低(P<0.01,P<0.05).与空白对照组比较,除了电针2组外,其余两组SR-BI、PPAR7均有显著降低(P<0.05,P<0.01);与模型对照组比较,电针1组和电针2组的SR-BI、PPARγ均有显著升高(P<0.05,P<0.01),其中电针2组更为显著(P<0.01).与空白对照组比较,除电针2组外,模型对照组和电针1组的炎症因子ICAM-1、IL-1β均有显著性升高(P<0.05,P<0.01),而模型对照组的抗炎因子IL-10有显著下降(P<0.01);与模型对照组比较,电针1组和电针2组的炎症因子ICAM-1、IL-1β均有非常显著性减少(P<0.01),而抗炎因子IL-10的含量有非常显著性升高(p<0.01).结论:通过电针丰隆穴治疗能降低高脂血症模型大鼠的TC、LDL-C水平,升高HDL-C水平,增加肝脏SR-BI、PPARγmRNA相对表�
