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目的:研究短时大量吸烟对长期吸烟者和不吸烟者血浆高密度脂蛋白(HDL)抗氧化、抗趋化和介导胆固醇外流能力的影响。方法:20例不吸烟者(不吸烟组)和10例长期吸烟健康受试者(长期吸烟组)短期大量吸烟(2小时内吸8支烟)前后,测定HDL抗铜离子诱导脂蛋白氧化的能力(以氧化迟滞时间表示)、改善巨噬细胞趋化性的能力(以细胞迁移数表示)以及HDL介导的巨噬细胞内NBD-胆固醇外流率的变化。结果:不吸烟组和长期吸烟组短时大量吸烟后HDL抗氧化能力均显著下降[氧化迟滞时间缩短,不吸烟组:(93.8±10.8)分比(88.5±10.8)分,P<0.05;长期吸烟组:(115.2±19.0)分比(89.4±20.3)分,P<0.05],抗趋化能力也均下降(细胞迁移数增多,不吸烟组:5.7±3.1比7.3±3.5×104,P<0.05;长期吸烟组:5.5±2.3比6.4±2.4×104,P>0.05),但两组人群短时大量吸烟前后HDL介导的胆固醇外流率均没有明显改变(不吸烟组:0.187±0.062比0.215±0.069,P>0.05;长期吸烟组:0.291±0.063比0.280±0.060,P>0.05)。结论:短时大量吸烟可降低HDL的抗氧化和抗趋化能力。
Objective: To investigate the effect of short-term massive smoking on the anti-oxidation, anti-chemotaxis and cholesterol efflux of plasma HDL in long-term and non-smokers. Methods: HDL was isolated from copper-induced lipoprotein oxidation in 20 non-smokers (nonsmokers) and 10 long-term smokers (long-term smokers) for short-term smoking (8 cigarettes smoked within 2 hours) Capacity (expressed as oxidative latency), the ability to improve macrophage chemotaxis (expressed as cell migration numbers), and HDL-mediated changes in NBD-cholesterol efflux in macrophages. Results: The anti-oxidative capacity of HDL in non-smoker group and long-term smoker group was significantly decreased after a short period of heavy smoking (the oxidative retardation time was shortened, while the non-smoker group was (93.8 ± 10.8) vs (88.5 ± 10.8), P < Smoking group: (115.2 ± 19.0) points (89.4 ± 20.3) points, P <0.05], anti-chemotaxis also decreased (cell migration increased, non-smoking group: 5.7 ± 3.1 vs 7.3 ± 3.5 × 104, P <0.05; long-term smoking group: 5.5 ± 2.3 vs 6.4 ± 2.4 × 104, P> 0.05). However, there was no significant change in HDL-mediated cholesterol efflux before and after short-term smoking in both groups (no smoking group: 0.187 ± 0.062 Than 0.215 ± 0.069, P> 0.05; long-term smoking group: 0.291 ± 0.063 vs 0.280 ± 0.060, P> 0.05). Conclusion: Short-term heavy smoking can reduce HDL anti-oxidation and anti-chemotaxis.