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| 1 | 黄芪葛根汤对高脂血症大鼠的降血脂作用机制研究显示文摘目的探讨黄芪葛根汤对高脂血症大鼠的降脂作用机制。方法将50只SD大鼠随机分为正常组、模型组、阳性药组(阿托伐他汀钙片,5 mg·kg^(-1))及黄芪葛根汤低、高剂量组(5、10 g·kg^(-1)),每组10只。采用高脂饲料喂养大鼠复制高脂血症模型,模型复制的同时各给药组按照上述剂量灌胃给药,正常组和模型组给予等量生理盐水灌胃,每天1次,连续灌胃20 d。检测大鼠血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-c)和低密度脂蛋白胆固醇(LDL-c)水平;采用HE及油红染色观察大鼠肝脏病理变化;采用qPCR及Western Blot法检测小肠组织尼曼-匹克C1型类蛋白1(NPC1L1)、三磷酸腺苷结合盒转运蛋白G5(ABCG5)和三磷酸腺苷结合盒转运蛋白G8(ABCG8)mRNA及蛋白表达水平。结果与正常组比较,模型组大鼠血清TC、TG、LDL-c水平及小肠组织NPC1L1 mRNA及蛋白表达水平明显升高(P<0.01,P<0.05),HDL-c水平明显降低(P<0.01),肝细胞脂肪变性程度和脂滴积聚明显增加。与模型组比较,黄芪葛根汤低剂量组大鼠血清TC、TG、LDL-c水平与小肠组织NPC1L1 mRNA及蛋白表达水平明显降低(P<0.01,P<0.05),ABCG5、ABCG8 mRNA及蛋白表达水平明显升高(P<0.01,P<0.05),肝细胞脂肪变性程度明显降低,脂滴积聚明显减少。结论黄芪葛根汤对高脂血症大鼠具有明显降血脂作用,能降低肝细胞脂肪变性程度和减少肝细胞脂滴积聚,可能与其下调小肠组织NPC1L1的表达以抑制胆固醇的吸收,同时上调小肠组织ABCG5及ABCG8的表达而增加胆固醇的排泄有关。 | 周遵明 谭梅傲 彭冲 于小庆 叶晋通 凡思敏 柯雪红 黄可儿 | 2021 | 中药新药与临床药理2021，32，7： | 16 |
| 2 | 调脂药物的作用靶点显示文摘血脂异常是动脉粥样硬化、冠心病等心血管疾病的重要危险因素,调脂药物治疗的主要目标是降低血浆低密度脂蛋白,升高高密度脂蛋白。尼曼-匹克C1型类似蛋白1(NPC1L1),胆固醇酰基转移酶(ACAT),三磷酸腺苷结合盒转运体G5和G8(ABCG5/G8),微粒体三酰甘油转运蛋白(MTP),单酰基甘油酰基转移酶(MAGT),二酰基甘油酰基转移酶(DAGT),过氧化物酶体增生激活型受体(PPAR),法尼醇X受体(FXR),前蛋白转化酶枯草溶菌素9(PCSK9)等是参与血脂代谢的重要蛋白,也是调脂药物作用相关的靶点,在调脂药物的开发和临床用药选择上具有重要参考价值。 | 李慧 景贤 邓晓兰 欧阳冬生 | 2013 | 中南大学学报(医学版)2013，38，1： | 13 |
| 3 | 大黄灵仙胶囊调控胆结石小鼠肝细胞转运蛋白表达及胆汁代谢谱的机制研究显示文摘目的通过Western blot法和气相色谱-质谱(GC-MS)联用技术观察大黄灵仙胶囊对小鼠胆结石肝细胞转运蛋白表达及胆汁代谢谱的影响,探讨其可能机制。方法将50只雄性C57BL/6小鼠随机分为正常对照组(N组)、模型组(M组)、熊去氧胆酸(UDCA)对照组(U组)、药物对照组(Y组)及大黄灵仙胶囊治疗组(D组),每组10只。N组和Y组小鼠普通饲料喂养,M、U、D组给予高脂、高热量、高胆固醇饲料诱导胆囊结石的形成。同时U组每天给予130mg/kg UDCA溶液灌胃;Y组和D组每天给予大黄灵仙胶囊汤药13g/kg灌胃,N组和M组给予相同体积的生理盐水灌胃。干预8周后,观察小鼠成石率,利用Western blot法观察肝胆管侧膜细胞转运蛋白三磷酸腺苷结合盒转运子B亚族成员11(ATP binding cassette subfamily B member 11,Abcb11)和三磷酸腺苷结合盒转运体c2(ATP binding cassette subfamily C member 2,Abcc2)变化,GC-MS技术检测小鼠胆汁代谢组学特征。结果造模期间因灌胃操作不慎,U组1只小鼠挣扎时灌胃针扎破小鼠食管导致死亡。M组成石率为100.00%,高于N组和Y组(均为0.00%,χ2=20.00,P<0.01);与M组比较,U组及D组成石率降低(44.44%,χ2=7.54,P=0.011;30.00%,χ2=10.77,P=0.003)。经红外光谱分析检测后在2939、1 446、1 382、1 056cm-1处可见胆固醇特有吸收峰。5组小鼠Abcb11和Abcc2转运蛋白总体比较差异有统计学意义(F=41.89;P<0.01;F=90.01,P<0.01)。与N组比较,M组Abcb11和Abcc2表达降低(P<0.01);与M组比较,U、Y、D组转运蛋白Abcb11和Abcc2表达均升高(P<0.01)。与其他组比较,模型组小鼠胆汁内源性代谢物丙氨酸、柠檬酸、赖氨酸、蛋氨酸、苯丙氨酸、酪氨酸、胆固醇、LDL、甘油、苹果酸及丙酮浓度升高,乳酸、谷氨酰、胺甘氨酸、胆碱及牛磺酸浓度降低,差异有统计学意义(P<0.05,P<0.01)。结论大黄灵仙胶囊具有稳定肝胆管侧膜细胞转运蛋白表达、改变或改善病理性胆汁的分泌及其代谢物的作用,从而达到防治胆结石的目的。 | 唐乾利 吕震 俞渊 王兵 李辉 金萌 王宇 王澍 | 2016 | 中国中西医结合杂志2016，36，8： | 13 |
| 4 | 瘦素对血脂及胆汁成分的调节在胆囊胆固醇结石形成中的作用显示文摘目的:分析胆囊胆固醇结石患者瘦素与血脂及胆囊内胆汁成分的关系,探讨瘦素在胆囊胆固醇结石形成中的作用。方法:选择胆囊胆固醇结石接受腹腔镜胆囊切除术的患者30例(结石组)与同期因胆囊息肉行腹腔镜胆囊切除术的患者22例(息肉组),检测患者血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、瘦素、胆囊胆汁中的TC与总胆汁酸(TBA)水平,以及胆囊壁组织瘦素受体mRNA水平。结果:与息肉组比较,结石组血清TC、TG、LDL、瘦素水平以及胆囊内胆汁TC/TBA含量比率与胆囊组织瘦素受体mRNA水平均明显升高,而血清HDL明显降低(均P<0.05)。结石组的血清瘦素水平与血清TG、TC及胆汁TC均呈正相关(r=0.633,P=0.002;r=0.224,P=0.025;r=0.384,P=0.000),与HDL和TBA呈负相关(r=-0.205,P=0.014;r=-0.548,P=0.024)呈负相关,而息肉组血清瘦素与以上指标间均无关(均P>0.05)。结论:瘦素参与了胆囊胆固醇结石的形成,瘦素及其受体水平的升高可能与胆囊胆固醇结石患者胆固醇代谢异常、胆囊胆汁成分失调密切相关。 | 郭怀斌 潘毓 暴雷 王春城 张万星 | 2018 | 中国普通外科杂志2018，27，2： | 10 |
| 5 | 抗高脂血症:新靶点与新药研发显示文摘高脂血症是引发各种心脑血管疾病最主要的因素之一,通过调节血脂来降低心脑血管疾病的发生率,具有重大意义。从调控内源性脂质合成、外源性脂质吸收与胆汁酸重吸收、血浆脂蛋白代谢以及脂质代谢等4个方面出发,系统概述抗高脂血症的新靶点与新药研究进展,旨在为高脂血症的治疗药物开发提供参考。 | 阮文臣 张天宁 李佳 张陆勇 庞涛 | 2017 | 药学进展2017，41，1： | 10 |
| 6 | 胆固醇的代谢调控与细胞内运输机制显示文摘中国科协生命科学学会联合体:胆固醇是细胞不可或缺的脂类物质,其代谢异常会引起动脉粥样硬化和神经系统病变。胆固醇不溶于水,其在细胞内运输机制并不清楚。武汉大学宋保亮团队研究发现,细胞内过氧化物酶体上的脂质分子Pl(4,5)P2与溶酶体Syt VII蛋白之间相互作用而产生动态接触。 | 廖雅成 宋保亮 | 2016 | 科技导报2016，34，13： | 8 |
| 7 | 胆囊胆固醇结石相关基因的研究进展显示文摘胆固醇结石的形成是多基因综合作用的结果,受遗传和环境等多方面综合因素的影响。COX-2参与胆囊结石成核因子,与胆固醇合成酶活性、胆囊炎症反应等有关,促使胆囊结石的形成;将45条胆囊胆固醇结石病的候选基因分为6大类,此些基因主要编码脂类代谢相关蛋白及胆囊相关蛋白;目前共发现了23个Lith基因被确认与胆囊结石有关。 | 布和 何涛 | 2013 | 包头医学院学报2013，29，6： | 1 |
| 8 | Isolation and biochemical analysis of vesicles from taurohyodeoxycholic acid-infused isolated perfused rat livers显示文摘AIM:To isolate biliary lipid-carrying vesicles from isolated perfused rat livers after taurohyodeoxycholic acid(THDC)infusion.Biliary lipid vesicles have been implicated in hepatic disease and THDC was used since it increases biliary phospholipid secretion.METHODS:Rat livers were isolated and perfused via the hepatic portal vein with THDC dissolved in Krebs Ringer Bicarbonate solution,pH 7.4,containing 1 mmol/L CaCl2,5 mmol/L glucose,a physiological amino acid mixture,1%bovine serum albumin and 20%(v/v)washed human erythrocytes at a rate of 2000 nmol/min for 2h.The livers were then removed,homogenized and subjected to centrifugation,and the microsomal fraction was obtained and further centrifuged at 350000 g for 90 min to obtain subcellular fractions.These were analyzed for total phospholipid,cholesterol,protein and alkaline phosphodiesterase I(PDE).RESULTS:No significant changes were observed in the total phospholipid,cholesterol and protein contents of the gradient fractions obtained from the microsomal preparation.However,the majority of the gradient fractions(ρ=1.05-1.07 g/mL andρ=1.95-1.23 g/mL)obtained from THDC-infused livers had significantly higher PDE activity compared to the control livers.The low density gradient fraction(ρ=1.05-1.07 g/mL)which was envisaged to contain the putative vesicle population isolated from THDC-perfused livers had relatively small amounts of phospholipids and protein when compared to the relevant control fractions;however,they displayed an increase in cholesterol and PDE activity.The phospholipids were also isolated by thin layer chromatography and subjected to fractionation by high performance liquid chromatography;however,no differences were observed in the pattern of the fatty acid composition of the phospholipids isolated from THDC and control perfused livers.The density gradient fractions(ρ=1.10-1.23 g/mL)displayed an increase in all the parameters measured from both control and THDCinfused livers.CONCLUSION:No significant changes in biliary lipids were observed in the fractions from THDC-infused livers;however,PDE activity was significantly increased compared to the control livers. | Adnan Adil Hismiogullari Sahver Ege Hismiogullari Khalid Rahman | 2013 | World Journal of Gastroenterology2013，19，37： | 0 |
| 9 | New insights into the role of Lith genes in the formation of cholesterol-supersaturated bile显示文摘Cholesterol gallstone formation represents a failure of biliary cholesterol homeostasis in which the physical-chemical balance of cholesterol solubility in bile is disturbed.Lithogenic bile is mainly caused by persistent hepatic hypersecretion of biliary cholesterol and sustained cholesterol-supersaturated bile is an essential prerequisite for the precipitation of solid cholesterol monohydrate crystals and the formation of cholesterol gallstones.The metabolic determinants of the supply of hepatic cholesterol molecules that are recruited for biliary secretion are dependent upon the input-output balance of cholesterol and its catabolism in the liver.The sources of cholesterol for hepatic secretion into bile have been extensively investigated;however,to what extent each cholesterol source contributes to hepatic secretion is still unclear both under normal physiological conditions and in the lithogenic state.Although it has been long known that biliary lithogenicity is initiated by hepatic cholesterol hypersecretion,the genetic mechanisms that cause supersaturated bile have not been defined yet.Identification of the Lith genes that determine hepatic cholesterol hypersecretion should provide novel insights into the primary genetic and pathophysiological defects for gallstone formation.In this review article,we focus mainly on the pathogenesis of the formation of supersaturated bile and gallstones from the viewpoint of genetics and pathophysiology.A better understanding of the molecular genetics and pathophysiology of the formation of cholesterol-supersaturated bile will undoubtedly facilitate the development of novel,effective,and noninvasive therapies for patients with gallstones,which would reduce the morbidity,mortality,and costs of health care associated with gallstones,a very prevalent liver disease worldwide. | Helen H.Wang Tiangang Li Piero Portincasa David A.Ford Brent A.Neuschwander-Tetri Patrick Tso David Q-H.Wang | 2017 | Liver Research2017，1，1： | 0 |
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