吸烟对巨噬细胞胆固醇逆转运影响的在体和离体研究
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摘要
背景
吸烟是动脉粥样硬化和冠心病发病的独立危险因素。吸烟影响动脉粥样硬化发生、发展的多个环节,可以导致血管内皮功能紊乱,促进炎症和氧化应激的产生,引起血脂代谢异常以及促进血栓形成。但是,吸烟促进动脉粥样硬化发生的确切机制目前仍不清楚。动脉粥样硬化的形成是一个复杂的病理生理过程。胆固醇在巨噬细胞中过量聚集形成泡沫细胞,这是动脉粥样硬化斑块的主要细胞成分及特征性的病理改变。胆固醇逆转运是将外周组织(包括动脉粥样硬化斑块)中过多的胆固醇转运至肝脏,进而以粪便的形式被排出体外的过程。因此,胆固醇逆转运可以减少胆固醇在血管壁沉积和抑制动脉粥样硬化斑块的形成。胆固醇逆转运是一个复杂的动态平衡过程。胆固醇流出是巨噬细胞胆固醇逆转运的第一步,也是其限速步骤。胆固醇流出依赖于胆固醇转运体腺苷三磷酸结合盒转运体A1 (ABCA1)、腺苷三磷酸结合盒转运体G1 (ABCG1)、清道夫受体B1 (SR-B1)的表达水平以及细胞外接受体高密度脂蛋白(HDL)的浓度和组成。胆固醇在肝脏中转化为胆汁酸盐,最后经肠腔排出体外,这是胆固醇逆转运的最后步骤。腺苷三磷酸结合盒转运体G5 (ABCG5)和腺苷三磷酸结合盒转运体G8 (ABCG8)参与胆固醇的肝肠排泄,在巨噬细胞胆固醇逆转运中也起着重要作用。大量的研究表明,吸烟不仅可以降低HDL-C的血浆浓度,而且可以氧化修饰HDL,使HDL的抗动脉粥样硬化作用降低。此外,吸烟可以对ABCG5和ABCG8产生影响。但是,目前尚不清楚吸烟是否影响小鼠在体巨噬细胞胆固醇逆转运效率。
目的
本实验将小鼠被动吸烟8周,采用一种替代方法研究吸烟对小鼠在体巨噬细胞胆固醇逆转运的影响及其机制。并进一步研究吸烟组小鼠血清以及香烟烟雾提取物(CSE)对巨噬细胞胆固醇流出的影响及机制。
方法
14只雄性C57BL／6小鼠随机分为对照组和吸烟组。吸烟组小鼠被动吸烟8周后腹腔注射经乙酰化低密度脂蛋白(Ac-LDL)及3H-胆固醇处理过的小鼠巨噬细胞悬液,单独笼养48小时后收集小鼠血清、肝脏、胆汁和粪便。γ射线计数仪检测血清、肝脏、胆汁和粪便中3H-胆固醇的放射活性并计算其占腹腔注射总量的百分比。采用逆转录聚合酶链反应(RT-PCR)和Western blot法分别检测分别肝脏和小肠中ABCG5/ABCG8的mRNA和蛋白表达。小鼠巨噬细胞RAW264.7与终浓度为50μg/ml的Ac-LDL以及1μCi/ml的3H-胆固醇共同孵育24小时使巨噬细胞荷脂和标记,小鼠血清或香烟烟雾提取物作用于小鼠巨噬细胞,γ射线计数仪检测巨噬细胞内及细胞上清液中3H-胆固醇含量并计算胆固醇流出的效率。采用Western blot法检测巨噬细胞中ABCA1、ABCG1、SR-B1、肝X受体α(LXRα)和过氧化酶体增殖物活化受体γ(PPARγ)的蛋白表达水平。并探讨抗氧化剂N-乙酰半胱氨酸(NAC)或PPARγ的激动剂15-脱氧前列腺素J2 (15d-PGJ2)对巨噬细胞胆固醇流出的影响。
结果
1.吸烟组小鼠血清、肝脏、胆汁和粪便中3H-胆固醇的放射活性均显著降低。
2.吸烟组小鼠血清介导巨噬细胞胆固醇流出的效率显著降低。
3.吸烟组小鼠肝脏和小肠组织中ABCG5/ABCG8的mRNA和蛋白表达水平均显著下降。
4.吸烟组小鼠血清中HDL-C显著下降,甘油三酯’(TG)和丙二醛(MDA)均显著升高。
5.用抗氧化剂NAC预先作用于吸烟组小鼠血清1小时,可以显著增加吸烟组小鼠血清介导的巨噬细胞胆固醇流出的效率。
6.不同浓度的CSE作用于巨噬细胞24小时,巨噬细胞胆固醇流出的效率显著降低,且呈剂量依赖性。
7.不同浓度的CSE作用于巨噬细胞24小时,巨噬细胞中ABCA1、ABCG1、PPARγ和LXRα的蛋白表达水平显著降低,且呈剂量依赖性,而巨噬细胞中SR-B1的蛋白表达水平没有显著性差别。
8.预先将PPARγ激动剂15d-PGJ2作用于巨噬细胞1小时,可以显著性增加巨噬细胞胆固醇流出以及巨噬细胞中ABCA1、ABCG1和LXRα蛋白表达,而巨噬细胞中SR-B1的蛋白表达水平没有显著性差别。
结论
1.吸烟显著降低小鼠体内巨噬细胞胆固醇逆转运。
2.吸烟显著降低小鼠肝脏和小肠组织中ABCG5/ABCG8 mRNA和蛋白水平的表达。
3.吸烟降低小鼠血清介导的巨噬细胞胆固醇流出效率可能与其降低HDL胆固醇的水平以及促进HDL脂质过氧化有关。
4.CSE通过抑制PPARγ-LXRα通路,使胆固醇转运体ABCA1和ABCG1的蛋白表达水平降低,进而降低巨噬细胞胆固醇流出的效率。
5.吸烟降低小鼠体内巨噬细胞胆固醇逆转运的效率可能与吸烟降低巨噬细胞胆固醇流出以及降低小鼠肝脏和小肠组织中ABCG5/ABCG8的表达有关。
Background
Cigarette smoking is an independent risk factor for atherosclerosis and coronary heart disease. Numerous studies have demonstrated that cigarette smoking influences all phases of atherosclerosis, which has an impact on endothelial dysfunction, platelet activation, increasing oxidative stress and inflammation as well as alterations in the lipid profile. However, the exact mechanism by which cigarette smoking increases the risk of atherosclerosis is not completely clarified. The formation of atherosclerotic lesion is a complex process. The accumulation of excess cholesterol in macrophages contributes to form foam cells, which is the hallmark of the atherosclerotic lesion. Reverse cholesterol transport is a process by which cholesterol in peripheral tissues is transported to the liver for excretion in the bile and feces, which can reduce the cholesterol deposition in the vascular wall and prevent atherosclerotic plaque formation. Therefore, reverse cholesterol transport is thought to be a protective mechanism against atherosclerosis. Cholesterol efflux is the first and also the rate-limiting step in macrophages reverse cholesterol transport. The rate of cellular cholesterol efflux is dependent on the expression of cholesterol transporters ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), scavenger receptor B1 (SR-B1) and the composition and concentration of extracellular cholesterol acceptor high density lipoprotein (HDL). The final step of macrophages reverse cholesterol transport involve liver uptake of HDL-derived cholesterol and excretion in the bile and feces. ATP-binding cassette transporters G5 (ABCG5) and ATP-binding cassette transporters G8 (ABCG8) heterodimerize into a functional complex ABCG5/G8 that is crucial for hepatobiliary and intestinal sterol excretion. Therefore, ABCG5/G8 also plays an important role in macrophages reverse cholesterol transport. Numerous studies have' demonstrated that cigarette smoking can decrease HDL cholesterol concentration and promote HDL to be oxidatively modified. In addition, cigarette smoking has an impact on ABCG5 and ABCG8. However, it is not clear whether cigarette smoking impairs macrophages reverse cholesterol transport in vivo.
Objective
A surrogate approach was developed to measure macrophages reverse cholesterol transport after the C57BL/6J mice were exposed to cigarette smoke for 8 weeks. The aim of this study was to study the effects of cigarette smoking on macrophages reverse cholesterol transport in vivo and the potential mechanisms. We also investigated the effects of mice serum and cigarette smoke extract (CSE) on macrophages cholesterol efflux and the potential mechanisms.
Methods
Fourteen healthy male C57BL/6 mice were randomly divided into control group and cigarette smoking group (n=7 each group). C57BL/6J mice were exposed to cigarette smoke for 8 weeks. We injected the mice intraperitoneally with 3H-cholesterol labeled and acetylated LDL (Ac-LDL) loaded macrophages. After 48 hours, serum, liver, bile and feces were collected for detecting the amounts of 3H-cholesterol. ABCG5 and ABCG8 mRNA and protein expressions in liver and intestine were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot respectively. RAW264.7 macrophages were labeled and loaded identically with media containing Ac-LDL (50μg/ml) and 3H-cholesterol (1μCi/ml) for 24 hours. RAW264.7 macrophages were treated with mice serum or different concentrations of CSE. We determined the rate of macrophages cholesterol efflux mediated by liquid scintillation counting. We also detected the protein expressions of ABCA1, ABCG1, SR-B1, liver X receptorα(LXRα) and peroxisome proliferator-activated receptorγ(PPARγ) in macrophages by western blot. We also determined the effect of N-acetylcysteine (NAC) or PPARγagonist 15d-PGJ2 on macrophages cholesterol efflux and cholesterol transporters.
Results
1. Compared with the control group, the amounts of 3H-cholesterol in serum, liver, bile and feces were significantly decreased in cigarette smoking group.
2. The rate of macrophages cholesterol efflux to mice serum was significantly decreased in cigarette smoking group than that in control group.
3. Compared with control group, ABCG5 and ABCG8 mRNA and protein expressions in liver and intestine were significantly decreased in cigarette smoking group.
4. After the C57BL/6J mice were exposed to cigarette smoke for 8 weeks, the mice of cigarette smoking group had lower HDL cholesterol, while had higher serum triglycerides (TG) and maleic dialdehyde (MDA) than those of the control group.
5. Pretreatment the antioxidant NAC with the serum from cigarette smoking group for 1 hour, NAC significantly increased the rate of macrophages cholesterol efflux mediated by serum from the cigarette smoking group.
6. Treated with different concentrations of CSE for 24 hours, the macrophages cholesterol efflux mediated by HDL was dose-dependently decreased.
7. CSE with different concentrations dose-dependently decreased the protein expressions of ABCA1, ABCG1, LXRαand PPARγin macrophages. However, CSE had no effect on the protein expression of SR-B1.
8. Pretreatment with the PPARγagonist 15d-PGJ2 for 1 hour could significantly increased macrophages cholesterol efflux induced by 10% CSE. Compared with the 10% CSE group, PPARγagonist 15d-PGJ2 could significantly increase the protein expressions of ABCA1, ABCG1 and LXRαin macrophages. However,15d-PGJ2 had no effect on the protein expression of SR-B1.
Conclusions
1. Cigarette smoking impaired macrophages reverse cholesterol transport in mice.
2. Cigarette smoking decreased the mRNA and protein expression of ABCG5 and ABCG8 in liver and intestine of mice.
3. The effect of cigarette smoking decreasing macrophages cholesterol efflux mediated by mice serum was attributed to its effect on decreasing HDL cholesterol and its effect on promoting HDL to be oxidatively modified.
4. The effect of CSE on PPARγ-LXRαpathway could decrease the protein expressions of ABCA1 and ABCG1 in macrophages, which contributed to decrease macrophages cholesterol efflux.
5. The macrophages reverse cholesterol transport was decreased in cigarette smoking group, which was possibly attributed to the decreased macrophage cholesterol efflux mediated by mice serum and the decreased mRNA and protein expressions of ABCG5 and ABCG8 in liver and intestine.
吸烟是动脉粥样硬化和冠心病发病的独立危险因素。吸烟影响动脉粥样硬化发生、发展的多个环节,可以导致血管内皮功能紊乱,促进炎症和氧化应激的产生,引起血脂代谢异常以及促进血栓形成。但是,吸烟促进动脉粥样硬化发生的确切机制目前仍不清楚。动脉粥样硬化的形成是一个复杂的病理生理过程。胆固醇在巨噬细胞中过量聚集形成泡沫细胞,这是动脉粥样硬化斑块的主要细胞成分及特征性的病理改变。胆固醇逆转运是将外周组织(包括动脉粥样硬化斑块)中过多的胆固醇转运至肝脏,进而以粪便的形式被排出体外的过程。因此,胆固醇逆转运可以减少胆固醇在血管壁沉积和抑制动脉粥样硬化斑块的形成。胆固醇逆转运是一个复杂的动态平衡过程。胆固醇流出是巨噬细胞胆固醇逆转运的第一步,也是其限速步骤。胆固醇流出依赖于胆固醇转运体腺苷三磷酸结合盒转运体A1 (ABCA1)、腺苷三磷酸结合盒转运体G1 (ABCG1)、清道夫受体B1 (SR-B1)的表达水平以及细胞外接受体高密度脂蛋白(HDL)的浓度和组成。胆固醇在肝脏中转化为胆汁酸盐,最后经肠腔排出体外,这是胆固醇逆转运的最后步骤。腺苷三磷酸结合盒转运体G5 (ABCG5)和腺苷三磷酸结合盒转运体G8 (ABCG8)参与胆固醇的肝肠排泄,在巨噬细胞胆固醇逆转运中也起着重要作用。大量的研究表明,吸烟不仅可以降低HDL-C的血浆浓度,而且可以氧化修饰HDL,使HDL的抗动脉粥样硬化作用降低。此外,吸烟可以对ABCG5和ABCG8产生影响。但是,目前尚不清楚吸烟是否影响小鼠在体巨噬细胞胆固醇逆转运效率。
目的
本实验将小鼠被动吸烟8周,采用一种替代方法研究吸烟对小鼠在体巨噬细胞胆固醇逆转运的影响及其机制。并进一步研究吸烟组小鼠血清以及香烟烟雾提取物(CSE)对巨噬细胞胆固醇流出的影响及机制。
方法
14只雄性C57BL／6小鼠随机分为对照组和吸烟组。吸烟组小鼠被动吸烟8周后腹腔注射经乙酰化低密度脂蛋白(Ac-LDL)及3H-胆固醇处理过的小鼠巨噬细胞悬液,单独笼养48小时后收集小鼠血清、肝脏、胆汁和粪便。γ射线计数仪检测血清、肝脏、胆汁和粪便中3H-胆固醇的放射活性并计算其占腹腔注射总量的百分比。采用逆转录聚合酶链反应(RT-PCR)和Western blot法分别检测分别肝脏和小肠中ABCG5/ABCG8的mRNA和蛋白表达。小鼠巨噬细胞RAW264.7与终浓度为50μg/ml的Ac-LDL以及1μCi/ml的3H-胆固醇共同孵育24小时使巨噬细胞荷脂和标记,小鼠血清或香烟烟雾提取物作用于小鼠巨噬细胞,γ射线计数仪检测巨噬细胞内及细胞上清液中3H-胆固醇含量并计算胆固醇流出的效率。采用Western blot法检测巨噬细胞中ABCA1、ABCG1、SR-B1、肝X受体α(LXRα)和过氧化酶体增殖物活化受体γ(PPARγ)的蛋白表达水平。并探讨抗氧化剂N-乙酰半胱氨酸(NAC)或PPARγ的激动剂15-脱氧前列腺素J2 (15d-PGJ2)对巨噬细胞胆固醇流出的影响。
结果
1.吸烟组小鼠血清、肝脏、胆汁和粪便中3H-胆固醇的放射活性均显著降低。
2.吸烟组小鼠血清介导巨噬细胞胆固醇流出的效率显著降低。
3.吸烟组小鼠肝脏和小肠组织中ABCG5/ABCG8的mRNA和蛋白表达水平均显著下降。
4.吸烟组小鼠血清中HDL-C显著下降,甘油三酯’(TG)和丙二醛(MDA)均显著升高。
5.用抗氧化剂NAC预先作用于吸烟组小鼠血清1小时,可以显著增加吸烟组小鼠血清介导的巨噬细胞胆固醇流出的效率。
6.不同浓度的CSE作用于巨噬细胞24小时,巨噬细胞胆固醇流出的效率显著降低,且呈剂量依赖性。
7.不同浓度的CSE作用于巨噬细胞24小时,巨噬细胞中ABCA1、ABCG1、PPARγ和LXRα的蛋白表达水平显著降低,且呈剂量依赖性,而巨噬细胞中SR-B1的蛋白表达水平没有显著性差别。
8.预先将PPARγ激动剂15d-PGJ2作用于巨噬细胞1小时,可以显著性增加巨噬细胞胆固醇流出以及巨噬细胞中ABCA1、ABCG1和LXRα蛋白表达,而巨噬细胞中SR-B1的蛋白表达水平没有显著性差别。
结论
1.吸烟显著降低小鼠体内巨噬细胞胆固醇逆转运。
2.吸烟显著降低小鼠肝脏和小肠组织中ABCG5/ABCG8 mRNA和蛋白水平的表达。
3.吸烟降低小鼠血清介导的巨噬细胞胆固醇流出效率可能与其降低HDL胆固醇的水平以及促进HDL脂质过氧化有关。
4.CSE通过抑制PPARγ-LXRα通路,使胆固醇转运体ABCA1和ABCG1的蛋白表达水平降低,进而降低巨噬细胞胆固醇流出的效率。
5.吸烟降低小鼠体内巨噬细胞胆固醇逆转运的效率可能与吸烟降低巨噬细胞胆固醇流出以及降低小鼠肝脏和小肠组织中ABCG5/ABCG8的表达有关。
Background
Cigarette smoking is an independent risk factor for atherosclerosis and coronary heart disease. Numerous studies have demonstrated that cigarette smoking influences all phases of atherosclerosis, which has an impact on endothelial dysfunction, platelet activation, increasing oxidative stress and inflammation as well as alterations in the lipid profile. However, the exact mechanism by which cigarette smoking increases the risk of atherosclerosis is not completely clarified. The formation of atherosclerotic lesion is a complex process. The accumulation of excess cholesterol in macrophages contributes to form foam cells, which is the hallmark of the atherosclerotic lesion. Reverse cholesterol transport is a process by which cholesterol in peripheral tissues is transported to the liver for excretion in the bile and feces, which can reduce the cholesterol deposition in the vascular wall and prevent atherosclerotic plaque formation. Therefore, reverse cholesterol transport is thought to be a protective mechanism against atherosclerosis. Cholesterol efflux is the first and also the rate-limiting step in macrophages reverse cholesterol transport. The rate of cellular cholesterol efflux is dependent on the expression of cholesterol transporters ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), scavenger receptor B1 (SR-B1) and the composition and concentration of extracellular cholesterol acceptor high density lipoprotein (HDL). The final step of macrophages reverse cholesterol transport involve liver uptake of HDL-derived cholesterol and excretion in the bile and feces. ATP-binding cassette transporters G5 (ABCG5) and ATP-binding cassette transporters G8 (ABCG8) heterodimerize into a functional complex ABCG5/G8 that is crucial for hepatobiliary and intestinal sterol excretion. Therefore, ABCG5/G8 also plays an important role in macrophages reverse cholesterol transport. Numerous studies have' demonstrated that cigarette smoking can decrease HDL cholesterol concentration and promote HDL to be oxidatively modified. In addition, cigarette smoking has an impact on ABCG5 and ABCG8. However, it is not clear whether cigarette smoking impairs macrophages reverse cholesterol transport in vivo.
Objective
A surrogate approach was developed to measure macrophages reverse cholesterol transport after the C57BL/6J mice were exposed to cigarette smoke for 8 weeks. The aim of this study was to study the effects of cigarette smoking on macrophages reverse cholesterol transport in vivo and the potential mechanisms. We also investigated the effects of mice serum and cigarette smoke extract (CSE) on macrophages cholesterol efflux and the potential mechanisms.
Methods
Fourteen healthy male C57BL/6 mice were randomly divided into control group and cigarette smoking group (n=7 each group). C57BL/6J mice were exposed to cigarette smoke for 8 weeks. We injected the mice intraperitoneally with 3H-cholesterol labeled and acetylated LDL (Ac-LDL) loaded macrophages. After 48 hours, serum, liver, bile and feces were collected for detecting the amounts of 3H-cholesterol. ABCG5 and ABCG8 mRNA and protein expressions in liver and intestine were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot respectively. RAW264.7 macrophages were labeled and loaded identically with media containing Ac-LDL (50μg/ml) and 3H-cholesterol (1μCi/ml) for 24 hours. RAW264.7 macrophages were treated with mice serum or different concentrations of CSE. We determined the rate of macrophages cholesterol efflux mediated by liquid scintillation counting. We also detected the protein expressions of ABCA1, ABCG1, SR-B1, liver X receptorα(LXRα) and peroxisome proliferator-activated receptorγ(PPARγ) in macrophages by western blot. We also determined the effect of N-acetylcysteine (NAC) or PPARγagonist 15d-PGJ2 on macrophages cholesterol efflux and cholesterol transporters.
Results
1. Compared with the control group, the amounts of 3H-cholesterol in serum, liver, bile and feces were significantly decreased in cigarette smoking group.
2. The rate of macrophages cholesterol efflux to mice serum was significantly decreased in cigarette smoking group than that in control group.
3. Compared with control group, ABCG5 and ABCG8 mRNA and protein expressions in liver and intestine were significantly decreased in cigarette smoking group.
4. After the C57BL/6J mice were exposed to cigarette smoke for 8 weeks, the mice of cigarette smoking group had lower HDL cholesterol, while had higher serum triglycerides (TG) and maleic dialdehyde (MDA) than those of the control group.
5. Pretreatment the antioxidant NAC with the serum from cigarette smoking group for 1 hour, NAC significantly increased the rate of macrophages cholesterol efflux mediated by serum from the cigarette smoking group.
6. Treated with different concentrations of CSE for 24 hours, the macrophages cholesterol efflux mediated by HDL was dose-dependently decreased.
7. CSE with different concentrations dose-dependently decreased the protein expressions of ABCA1, ABCG1, LXRαand PPARγin macrophages. However, CSE had no effect on the protein expression of SR-B1.
8. Pretreatment with the PPARγagonist 15d-PGJ2 for 1 hour could significantly increased macrophages cholesterol efflux induced by 10% CSE. Compared with the 10% CSE group, PPARγagonist 15d-PGJ2 could significantly increase the protein expressions of ABCA1, ABCG1 and LXRαin macrophages. However,15d-PGJ2 had no effect on the protein expression of SR-B1.
Conclusions
1. Cigarette smoking impaired macrophages reverse cholesterol transport in mice.
2. Cigarette smoking decreased the mRNA and protein expression of ABCG5 and ABCG8 in liver and intestine of mice.
3. The effect of cigarette smoking decreasing macrophages cholesterol efflux mediated by mice serum was attributed to its effect on decreasing HDL cholesterol and its effect on promoting HDL to be oxidatively modified.
4. The effect of CSE on PPARγ-LXRαpathway could decrease the protein expressions of ABCA1 and ABCG1 in macrophages, which contributed to decrease macrophages cholesterol efflux.
5. The macrophages reverse cholesterol transport was decreased in cigarette smoking group, which was possibly attributed to the decreased macrophage cholesterol efflux mediated by mice serum and the decreased mRNA and protein expressions of ABCG5 and ABCG8 in liver and intestine.
引文
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