以脂代谢相关受体为靶点的抗动脉粥样硬化药物筛选及药物作用机制研究
摘要
目前,心脑血管疾病是世界发病率最高的疾病之一,其致死、致残率高居各类疾病之首。其中,动脉粥样硬化(Atherosclerosis,AS)的发生是心脑血管疾病的主要病理基础。脂质代谢紊乱尤其是胆固醇代谢紊乱是目前公认的主要致病因子。调脂药物的早期研究主要集中于针对低密度脂蛋白受体(low densitylipoprotein receptor,LDLR)通路,他汀类药物是其代表药物,具有出色的降胆固醇疗效,可明显降低心脏病及卒中的风险。但是他汀类药物总的有效率仅为20～40%,因此,心血管疾病远未解决,亟需发现新作用机制的药物。近年来,在新型调脂药物研发过程中,血浆脂蛋白代谢过程中的另两个关键步骤:胆固醇逆向转运(reverse cholesterol transport,RCT)通路及泡沫细胞形成(foam cellformation)过程受到越来越多的关注。本论文围绕着这两个方面开展了相关药物筛选和作用机制研究。
高密度脂蛋白(high density lipoprotein,HDL)是胆固醇逆向转运中最主要的胆固醇携带者,在这一过程中,B族I型清道夫受体SR-BI(人的同源基因命名为CLA-1)发挥了重要作用。作为HDL的受体,SR-BI参与调节肝脏对脂质的选择性摄取,介导HDL胆固醇酯选择性进入细胞;另外,在外周细胞,SR-BI能通过结合HDL促进胆固醇的外流。由于SR-BI在RCT的起始及终末步骤中都发挥了重要作用,因此被认为是抗动脉粥样硬化药物的潜在靶点之一。本研究室构建了基于细胞的高密度脂蛋白受体表达上调剂高通量筛选模型,对化合物及微生物次级代谢产物进行了大规模筛选,其中阳性菌株04-9179可有效上调CLA-1启动子的活性,从该菌株发酵液中分离得到阳性化合物9179A及阳性组分B和C。
本论文第一部分针对CLA-1表达上调剂9179A进行结构确证,活性检测及相关分子作用机制研究。在前期工作基础上,经化学及生物学分析进一步确证,9179A为已知化合物Trichostatin A。检测9179A对人肝癌细胞HepG2及小鼠巨噬细胞RAW 264.7中CLA-1/SR-BI表达水平的影响,结果表明9179A可分别上调HepG2及RAW 264.7中CLA-1/SR-BI mRNA及蛋白水平。在此基础上,进一步检测9179A对HepG2和RAW 264.7细胞的脂质摄取能力以及RAW 264.7细胞胆固醇外流能力的影响,结果表明,9179A可上调HepG2细胞和RAW 264.7细胞对DiI-HDL的摄取,还可上调RAW 264.7细胞的胆固醇外流能力。对9179A分子作用机制的进一步研究提示,9179A可能通过调控含有SRE/SP1等顺式元件的启动子区域发挥上调CLA-1/SR-BI转录的作用。此外,我们还对阳性菌株04-9179中阳性组分B和C进行了分离纯化、结构鉴定和活性测定,结果表明,化合物9179B和9179C对CLA-1启动子活性的上调作用较低。
细胞泡沫化是AS形成的关键步骤。巨噬细胞上存在的清道夫受体A(SR-A)和B族清道夫受体CD36可导致oxLDL被细胞无限制摄取(即在摄取时不受负反馈调控),因此它们在泡沫细胞形成中发挥重要作用。体内、外研究显示,60～90%的巨噬细胞泡沫化是由CD36介导的。因此CD36被认为是抗动脉粥样硬化药物的潜在靶点之一。
在本论文第二部分中,我们在大肠杆菌中成功表达了重组CD36可溶性受体蛋白,并以此为靶点建立了CD36拮抗剂高通量筛选模型。分别扩增人CD36全长及可溶性片段(sCD36)cDNA,将它们克隆至pGEM-T载体并测序,分别与大肠杆菌表达载体pET-30a(+)连接,构建CD36及sCD36的重组表达质粒,并将重组质粒分别转化大肠杆菌表达宿主BL21(DE3),表达目的蛋白。经SDS-PAGE及Western Blot检测获得成功表达sCD36的重组菌株E.coliBL21(DE3)/pET-sCD36。该菌株表达的sCD36蛋白经配基结合实验及油红O染色实验证实具有配基结合活性。随后,利用该重组蛋白建立并优化了基于受体-配基竞争性结合的ELISA-like高通量药物筛选模型,并应用此模型筛选化合物640个。其中,具有抑制CD36配基结合活性的阳性化合物27个,阳性率为4.22%。对部分阳性化合物进行了活性验证,结果显示,受试化合物在细胞水平上具有抑制RAW 264.7细胞摄取oxLDL及DiI-acLDL的能力,进一步证实了构建模型的可行性。
Atherosclerosis is a progressive disease that is characterized by the accumulation of lipid-rich plaques within the walls of arteries.Despite substantial therapeutic progress resulting from the widespread use of statins,which primarily lower plasma levels of low density lipoprotein(LDL) cholesterol,atherosclerosis is still one of the leading causes of mortality in industrialized and developing nations.In recent years,the reverse cholesterol transport(RCT) pathway and modified low density lipoprotein (mLDL) induced foam cell formation,two processes other than LDLR pathway were extensively studied and concerned as major targets for the development of novel therapies.
Plasma concentrations of high density lipoprotein(HDL) cholesterol(HDL-C) are inversely proportional to the risk for atherosclerotic cardiovascular disease.One of the major atheroprotective actions of HDL particles involves the transport of excess cholesterol from peripheral tissues to the liver for excretion,a process known as reverse cholesterol transport.Scavenger receptor class B typeⅠ(SR-BI) and its human homologue CLA-1 are the high-affinity HDL receptor.CLA-I/SR-BI,which plays an important role in reverse cholesterol transport,has been suggested as a new preventative and/or therapeutic target for atherosclerosis.
Using a previously established cell-based CLA-1 up-regulator screening assay,one of the positive strains,04-9179,presented potent activity in elevating CLA-1 transcriptional level.Three pure compounds,designated as 9179A,9179B and 9179C, were purified from the strain.The structures and bioactivities of these compounds were analyzed,and 9179A showed highest activity.9179A was demonstrated chemically and biologically identical to a known compound trichostatin A(TSA).The effects of 9179A on CLA-1/SR-BI expression both in HepG2 human hepatoma cells and RAW 264.7 murine macrophage cells were detected in vitro.The results showed that the mRNA and protein level of CLA-1/SR-BI were significantly up-regulated by 9179A both in HepG2 and RAW 264.7 cells.Corresponding to this,the uptake of fluorescent labeled-HDL(DiI-HDL) was increased by 9179A in dose-dependent manner in HepG2 and RAW 264.7 cells.The cholesterol efflux was also increased by 9179A in RAW 264.7 cells.Using a combination of reporter assays with various deletion in CLA-1 promoter and electrophoretic mobility shift assay,we demonstrated that -419～-232 bp fragment of the CLA-1 promoter mediated the effects of 9179A (i.e.,TSA).Combined treatment of CLAp-LUC HepG2 cells with 9179A and rosiglitazone(ROS) confirmed that they up-regulated the promoter activity through different cis-elements.Together,these studies identified a novel up-regulator of CLA-1/SR-BI both in HepG2 and RAW 264.7 cells,suggesting that TSA should be useful in further understanding of the transcriptional regulation of CLA-1/SR-BI,and might serve as a starting point for the development of novel antiatherosclerotic agents. Macrophage foam cell formation is a characteristic event that occurs in the early stage of atherosclerosis.A critical step in foam cell formation is recognition and internalization of oxidized low density lipoprotein(oxLDL) by scavenger receptors CD36 and SR-A.In ex vivo models it has been shown that 60～90%of macrophage foam cell formation may be CD36 dependent.In vivo studies of CD36-null mice showed a major negative impact of CD36 on lesion development.Extensive evidences point to a significant role of CD36 in atherosclerotic lesions and suggest that it could be a lead target for therapeutic treatment.
In this study,we constructed recombinant plasmid pET-sCD36 using pET-30a(+),and expressed soluble CD36(sCD36) in E.coli BL21(DE3).The protein of sCD36 was expressed in form of inclusion body and refolded by dilution.The ligand binding activity of sCD36 was validated by ligand binding assay and Oil Red O assay.With oxLDL itself as a positive control,sCD36 was used to establish a specific ELISA-like assay in a 96-well microplate format to screen CD36 antagonists.The conditions for the high-throughput screening(HTS) assay were optimized.The evaluating parameter Z' value of 0.84 showed that this cell-free HTS assay was robust and reliable. Screening of 640 chemical compounds identified 27 positive compounds.Active compounds were further validated by Oil Red O assay and DiI-acLDL uptake assay. The active compounds originated from this HTS assay may be developed to drug candidates or lead compounds for new antiatherosclerotic agents.
高密度脂蛋白(high density lipoprotein,HDL)是胆固醇逆向转运中最主要的胆固醇携带者,在这一过程中,B族I型清道夫受体SR-BI(人的同源基因命名为CLA-1)发挥了重要作用。作为HDL的受体,SR-BI参与调节肝脏对脂质的选择性摄取,介导HDL胆固醇酯选择性进入细胞;另外,在外周细胞,SR-BI能通过结合HDL促进胆固醇的外流。由于SR-BI在RCT的起始及终末步骤中都发挥了重要作用,因此被认为是抗动脉粥样硬化药物的潜在靶点之一。本研究室构建了基于细胞的高密度脂蛋白受体表达上调剂高通量筛选模型,对化合物及微生物次级代谢产物进行了大规模筛选,其中阳性菌株04-9179可有效上调CLA-1启动子的活性,从该菌株发酵液中分离得到阳性化合物9179A及阳性组分B和C。
本论文第一部分针对CLA-1表达上调剂9179A进行结构确证,活性检测及相关分子作用机制研究。在前期工作基础上,经化学及生物学分析进一步确证,9179A为已知化合物Trichostatin A。检测9179A对人肝癌细胞HepG2及小鼠巨噬细胞RAW 264.7中CLA-1/SR-BI表达水平的影响,结果表明9179A可分别上调HepG2及RAW 264.7中CLA-1/SR-BI mRNA及蛋白水平。在此基础上,进一步检测9179A对HepG2和RAW 264.7细胞的脂质摄取能力以及RAW 264.7细胞胆固醇外流能力的影响,结果表明,9179A可上调HepG2细胞和RAW 264.7细胞对DiI-HDL的摄取,还可上调RAW 264.7细胞的胆固醇外流能力。对9179A分子作用机制的进一步研究提示,9179A可能通过调控含有SRE/SP1等顺式元件的启动子区域发挥上调CLA-1/SR-BI转录的作用。此外,我们还对阳性菌株04-9179中阳性组分B和C进行了分离纯化、结构鉴定和活性测定,结果表明,化合物9179B和9179C对CLA-1启动子活性的上调作用较低。
细胞泡沫化是AS形成的关键步骤。巨噬细胞上存在的清道夫受体A(SR-A)和B族清道夫受体CD36可导致oxLDL被细胞无限制摄取(即在摄取时不受负反馈调控),因此它们在泡沫细胞形成中发挥重要作用。体内、外研究显示,60～90%的巨噬细胞泡沫化是由CD36介导的。因此CD36被认为是抗动脉粥样硬化药物的潜在靶点之一。
在本论文第二部分中,我们在大肠杆菌中成功表达了重组CD36可溶性受体蛋白,并以此为靶点建立了CD36拮抗剂高通量筛选模型。分别扩增人CD36全长及可溶性片段(sCD36)cDNA,将它们克隆至pGEM-T载体并测序,分别与大肠杆菌表达载体pET-30a(+)连接,构建CD36及sCD36的重组表达质粒,并将重组质粒分别转化大肠杆菌表达宿主BL21(DE3),表达目的蛋白。经SDS-PAGE及Western Blot检测获得成功表达sCD36的重组菌株E.coliBL21(DE3)/pET-sCD36。该菌株表达的sCD36蛋白经配基结合实验及油红O染色实验证实具有配基结合活性。随后,利用该重组蛋白建立并优化了基于受体-配基竞争性结合的ELISA-like高通量药物筛选模型,并应用此模型筛选化合物640个。其中,具有抑制CD36配基结合活性的阳性化合物27个,阳性率为4.22%。对部分阳性化合物进行了活性验证,结果显示,受试化合物在细胞水平上具有抑制RAW 264.7细胞摄取oxLDL及DiI-acLDL的能力,进一步证实了构建模型的可行性。
Atherosclerosis is a progressive disease that is characterized by the accumulation of lipid-rich plaques within the walls of arteries.Despite substantial therapeutic progress resulting from the widespread use of statins,which primarily lower plasma levels of low density lipoprotein(LDL) cholesterol,atherosclerosis is still one of the leading causes of mortality in industrialized and developing nations.In recent years,the reverse cholesterol transport(RCT) pathway and modified low density lipoprotein (mLDL) induced foam cell formation,two processes other than LDLR pathway were extensively studied and concerned as major targets for the development of novel therapies.
Plasma concentrations of high density lipoprotein(HDL) cholesterol(HDL-C) are inversely proportional to the risk for atherosclerotic cardiovascular disease.One of the major atheroprotective actions of HDL particles involves the transport of excess cholesterol from peripheral tissues to the liver for excretion,a process known as reverse cholesterol transport.Scavenger receptor class B typeⅠ(SR-BI) and its human homologue CLA-1 are the high-affinity HDL receptor.CLA-I/SR-BI,which plays an important role in reverse cholesterol transport,has been suggested as a new preventative and/or therapeutic target for atherosclerosis.
Using a previously established cell-based CLA-1 up-regulator screening assay,one of the positive strains,04-9179,presented potent activity in elevating CLA-1 transcriptional level.Three pure compounds,designated as 9179A,9179B and 9179C, were purified from the strain.The structures and bioactivities of these compounds were analyzed,and 9179A showed highest activity.9179A was demonstrated chemically and biologically identical to a known compound trichostatin A(TSA).The effects of 9179A on CLA-1/SR-BI expression both in HepG2 human hepatoma cells and RAW 264.7 murine macrophage cells were detected in vitro.The results showed that the mRNA and protein level of CLA-1/SR-BI were significantly up-regulated by 9179A both in HepG2 and RAW 264.7 cells.Corresponding to this,the uptake of fluorescent labeled-HDL(DiI-HDL) was increased by 9179A in dose-dependent manner in HepG2 and RAW 264.7 cells.The cholesterol efflux was also increased by 9179A in RAW 264.7 cells.Using a combination of reporter assays with various deletion in CLA-1 promoter and electrophoretic mobility shift assay,we demonstrated that -419～-232 bp fragment of the CLA-1 promoter mediated the effects of 9179A (i.e.,TSA).Combined treatment of CLAp-LUC HepG2 cells with 9179A and rosiglitazone(ROS) confirmed that they up-regulated the promoter activity through different cis-elements.Together,these studies identified a novel up-regulator of CLA-1/SR-BI both in HepG2 and RAW 264.7 cells,suggesting that TSA should be useful in further understanding of the transcriptional regulation of CLA-1/SR-BI,and might serve as a starting point for the development of novel antiatherosclerotic agents. Macrophage foam cell formation is a characteristic event that occurs in the early stage of atherosclerosis.A critical step in foam cell formation is recognition and internalization of oxidized low density lipoprotein(oxLDL) by scavenger receptors CD36 and SR-A.In ex vivo models it has been shown that 60～90%of macrophage foam cell formation may be CD36 dependent.In vivo studies of CD36-null mice showed a major negative impact of CD36 on lesion development.Extensive evidences point to a significant role of CD36 in atherosclerotic lesions and suggest that it could be a lead target for therapeutic treatment.
In this study,we constructed recombinant plasmid pET-sCD36 using pET-30a(+),and expressed soluble CD36(sCD36) in E.coli BL21(DE3).The protein of sCD36 was expressed in form of inclusion body and refolded by dilution.The ligand binding activity of sCD36 was validated by ligand binding assay and Oil Red O assay.With oxLDL itself as a positive control,sCD36 was used to establish a specific ELISA-like assay in a 96-well microplate format to screen CD36 antagonists.The conditions for the high-throughput screening(HTS) assay were optimized.The evaluating parameter Z' value of 0.84 showed that this cell-free HTS assay was robust and reliable. Screening of 640 chemical compounds identified 27 positive compounds.Active compounds were further validated by Oil Red O assay and DiI-acLDL uptake assay. The active compounds originated from this HTS assay may be developed to drug candidates or lead compounds for new antiatherosclerotic agents.
引文
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