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目的探讨三手烟对小鼠内皮祖细胞水平的影响及可能机制。方法 40只8周龄清洁级雄性小鼠,分为3组并做如下处理:对照组(n=10):暴露于正常空气中;一手烟组(n=15):每日接受香烟烟雾8 h;三手烟组(n=15):每日生活在香烟烟雾熏过的无菌敷料中8 h(无菌敷料接受同一手烟组一样的香烟烟雾烟熏8 h)。两个月后采血,测定并比较两组内皮祖细胞(endothelial progenitor cells,EPCs)、髓过氧化物酶(myeloperoxidase,MPO)、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、一氧化氮(nitric oxide,NO)水平。光镜下观察比较心肌组织学变化。结果一手烟组、三手烟组与对照组相比,EPCs百分比显著下降[分别(0.045±0.029)%vs.(0.099±0.023)%、(0.047±0.023)%vs.(0.099±0.023)%,均P<0.001],MPO、IL-6、TNF-α水平显著升高[分别为MPO:1.39±0.26)U/g vs.(0.48±0.17)U/g、(1.35±0.32)U/g vs.(0.48±0.17)U/g;IL-6:(3.83±0.13)ng/ml vs.(0.79±0.12)ng/ml、(3.45±0.15)ng/ml vs.(0.79±0.12)ng/ml;TNF-α:(1.77±0.26)ng/ml vs.(0.81±0.21)ng/ml、(1.78±0.23)ng/ml vs.(0.81±0.21)ng/ml,均P<0.001],NO水平显著降低[分别为(0.057±0.0063)μmol/L vs.(0.080±0.0067)μmol/L、(0.060±0.0072)μmol/L vs.(0.080±0.0067)μmol/L,均P<0.001];一手烟组、三手烟组比较各指标差异无统计学意义(均P>0.05),光镜下可见观察一手烟组、三手烟组与对照组相比心肌组织发生明显损伤。结论三手烟可通过氧化应激和炎症反应降低小鼠内皮祖细胞水平,损伤小鼠心肌组织,作用程度与一手烟相似。
Objective To explore the effect of third-hand smoke on the level of mouse endothelial progenitor cells and its possible mechanism. Methods Forty eight-week-old male mice were divided into 3 groups and treated as follows: Control group (n = 10): normal air exposure; h; Third-hand smoke group (n = 15): Daily living in aseptic dressings smoked by cigarette smoke for 8 h (aseptic dressings smoked cigarettes of the same smoker group for 8 h). Blood samples were taken two months later. The levels of endothelial progenitor cells (EPCs), myeloperoxidase (MPO), interleukin-6 (IL-6) Factor-α (TNF-α) and nitric oxide (NO) levels. Light microscopic observation of myocardial histological changes. Results Compared with the control group, the percentage of EPCs in the first-hand smoke group and the third-hand smoke group was significantly decreased (0.045 ± 0.029)% vs (0.099 ± 0.023)%, (0.047 ± 0.023)% vs (0.099 ± 0.023)% , P <0.001]. The levels of MPO, IL-6 and TNF-αwere significantly increased in MPO-treated mice as compared with those in control group (MPO: 1.39 ± 0.26 U / g vs. 0.48 ± 0.17 U / g, g vs. (0.48 ± 0.17) U / g; IL-6: 3.83 ± 0.13 ng / ml vs. 0.79 ± 0.12 ng / ml vs 3.79 ± 0.12 vs. 0.79 ± 0.12 (1.81 ± 0.21) ng / ml, (1.78 ± 0.23) ng / ml vs. (0.81 ± 0.21) ng / ml, all P <0.001 (P <0.05), and the level of NO significantly decreased (P <0.05). The levels of NO were significantly lower than those of the control group [(0.057 ± 0.0063) μmol / L vs. 0.080 ± 0.0067 μmol / L vs 0.060 ± 0.0072 μmol / L vs. 0.080 ± 0.0067 μmol / 0.001]. There was no significant difference between the first-hand smoke group and the third-hand smoke group (all P> 0.05). The light-microscope observation showed that the first-hand smoke group and the third-hand smoke group had obvious myocardial injury compared with the control group. Conclusion Third-hand smoke can reduce the level of endothelial progenitor cells and oxidative stress in mice, and damage the myocardium in mice. The degree of action is similar to that of first-hand smoke.