安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2015年
6期
757-760
,共4页
烟草暴露%戒烟%氧化应激%炎症因子
煙草暴露%戒煙%氧化應激%炎癥因子
연초폭로%계연%양화응격%염증인자
cigarette smoking exposure%smoking cessation%oxidative stress%inflammatory cytokines
目的：观察烟草暴露小鼠肺部氧化应激状态变化与炎症因子的关系及戒烟对其的影响。方法50只雄性Balb/ c 小鼠按随机数字表法分为对照组、烟雾暴露组、戒烟组。戒烟组小鼠烟雾暴露16周后戒烟，戒烟4、8、12周时处死小鼠留取支气管肺泡灌洗液（BALF）及肺组织标本。采用HE 法观察小鼠肺组织病理学形态改变，测量肺平均内衬间隔和平均肺泡数，收集 BALF 进行细胞计数，羟胺法测定肺组织匀浆中超氧化物歧化酶（SOD）活力，TBA 法测定肺匀浆中丙二醛（MDA）水平，ELISA 法测定 BALF 和肺匀浆中白细胞介素-8（IL-8）、肿瘤坏死因子-α（TNF-α）的浓度。结果与对照组比较，烟雾暴露组小鼠出现明显的肺气肿变化， BALF 中炎症细胞显著增多（P <0.05），戒烟后明显减少（P<0.05）；肺组织匀浆中 SOD 活力和 MDA 水平增高（ P <0.05），戒烟后逐渐下降。烟雾暴露组小鼠 BALF、肺组织匀浆中 IL-8和 TNF-α浓度显著增高（P <0.05），戒烟后明显降低，并随戒烟时间延长更加明显，但未降至正常水平。SOD活力和 MDA 水平与炎症因子之间呈显著正相关性。结论吸烟可以导致小鼠肺部氧化应激异常和气道炎症，戒烟可减轻氧化应激和气道炎症，但未能恢复到完全正常，炎症持续存在。
目的：觀察煙草暴露小鼠肺部氧化應激狀態變化與炎癥因子的關繫及戒煙對其的影響。方法50隻雄性Balb/ c 小鼠按隨機數字錶法分為對照組、煙霧暴露組、戒煙組。戒煙組小鼠煙霧暴露16週後戒煙，戒煙4、8、12週時處死小鼠留取支氣管肺泡灌洗液（BALF）及肺組織標本。採用HE 法觀察小鼠肺組織病理學形態改變，測量肺平均內襯間隔和平均肺泡數，收集 BALF 進行細胞計數，羥胺法測定肺組織勻漿中超氧化物歧化酶（SOD）活力，TBA 法測定肺勻漿中丙二醛（MDA）水平，ELISA 法測定 BALF 和肺勻漿中白細胞介素-8（IL-8）、腫瘤壞死因子-α（TNF-α）的濃度。結果與對照組比較，煙霧暴露組小鼠齣現明顯的肺氣腫變化， BALF 中炎癥細胞顯著增多（P <0.05），戒煙後明顯減少（P<0.05）；肺組織勻漿中 SOD 活力和 MDA 水平增高（ P <0.05），戒煙後逐漸下降。煙霧暴露組小鼠 BALF、肺組織勻漿中 IL-8和 TNF-α濃度顯著增高（P <0.05），戒煙後明顯降低，併隨戒煙時間延長更加明顯，但未降至正常水平。SOD活力和 MDA 水平與炎癥因子之間呈顯著正相關性。結論吸煙可以導緻小鼠肺部氧化應激異常和氣道炎癥，戒煙可減輕氧化應激和氣道炎癥，但未能恢複到完全正常，炎癥持續存在。
목적：관찰연초폭로소서폐부양화응격상태변화여염증인자적관계급계연대기적영향。방법50지웅성Balb/ c 소서안수궤수자표법분위대조조、연무폭로조、계연조。계연조소서연무폭로16주후계연，계연4、8、12주시처사소서류취지기관폐포관세액（BALF）급폐조직표본。채용HE 법관찰소서폐조직병이학형태개변，측량폐평균내츤간격화평균폐포수，수집 BALF 진행세포계수，간알법측정폐조직균장중초양화물기화매（SOD）활력，TBA 법측정폐균장중병이철（MDA）수평，ELISA 법측정 BALF 화폐균장중백세포개소-8（IL-8）、종류배사인자-α（TNF-α）적농도。결과여대조조비교，연무폭로조소서출현명현적폐기종변화， BALF 중염증세포현저증다（P <0.05），계연후명현감소（P<0.05）；폐조직균장중 SOD 활력화 MDA 수평증고（ P <0.05），계연후축점하강。연무폭로조소서 BALF、폐조직균장중 IL-8화 TNF-α농도현저증고（P <0.05），계연후명현강저，병수계연시간연장경가명현，단미강지정상수평。SOD활력화 MDA 수평여염증인자지간정현저정상관성。결론흡연가이도치소서폐부양화응격이상화기도염증，계연가감경양화응격화기도염증，단미능회복도완전정상，염증지속존재。
Objective To observe the changes of pulmonary oxidative stress after cigarette smoking exposure,its re-lationship with inflammatory cytokines,and the effects of smoking cessation. Methods Fifty male BALB / c mice were randomly divided into the smoke exposure group,smoke cessation group,and the controls. Mice in smoke cessation group were exposed to cigarette smoking for 16 weeks. On 4,8,and 12 week after smoking cessation mice were executed and the bronchoalveolar lavage fluid(BALF)and lung tissue were collected. The morphologi-cal alternations of lung tissue were observed. Mean length of interval and mean alveolar number were measured. Total cell numbers in BALF were counted. Superoxide dismutase(SOD)activity was measured with hydroxylamine method,malondialdehyde(MDA)level was measured with TBA method. The levels of pulmonary interleukin-8 (IL-8)and tumor necrosis factor-α(TNF-α)in BALF and lung tissue homogenate were measured with ELISA. Re-sults Compared with the mice in the controls,emphysematous changes were remarkable in the lung of cigarette ex-posed mice,the total cell numbers in BALF were increased significantly(P < 0. 05)and reduced gradually after smoking cessation(P < 0. 05). SOD and MDA levels increased remarkably in the cigarette exposure group(P <0. 05),and declined gradually after smoking cessation. The levels of IL-8 and TNF-α in BALF and lung tissue ho-mogenate in the smoke exposure group increased significantly( P < 0. 05),and lowered time-dependently after smoking cessation,but not reached to normal level even 12 weeks after smoking cessation. SOD and MDA levels were positively correlated with the cytokine changes. Conclusion Abnormal oxidative stress in the airways caused by cigarette smoking exposure was merely partially reversed after smoking cessation. And the inflammation remains persistent concomitantly.
