CAJ | 학술논문

目的： CD8＋T细胞在慢性阻塞性肺疾病患者气道中增多且持续存在，观察CD8＋T细胞在烟草烟雾暴露及脂多糖（ lipopolysaccharide ， LPS）诱导大鼠慢性支气管炎的膜性支气管表达以探讨CD8＋T细胞在慢性支气管炎中的作用。方法18只健康雄性Wistar大鼠按随机数字表法分为3组：假吸烟组、慢性支气管炎组、N-乙酰半胱氨酸（ acetylcysteine ， NAC）组，假吸烟组经气道注入等渗盐水，慢性支气管炎大鼠模型采用2次气管内注入LPS及烟熏4周法制备，NAC组在慢性支气管炎组基础上予NAC（200 mg／kg）灌胃干预。各组大鼠取肺组织HE染色观察膜性支气管的病理形态并进行炎症病变病理评分，核因子-κB（nuclear factorκB， NF-κB）、Ⅰ类主要相容性复合体（major histocompatibility complex class I ， MHC I）、CD8＋T细胞和血管内皮生长因子（vascular endothelial growth factor ， VEGF）免疫组化采用免疫组化SP法染色检测。结果假吸烟组、NAC组病理积分[1．17±2．40、4．66±2．25]均较慢性支气管炎组（10．83±3．31）明显降低（P ＜0．05），假吸烟组与NAC组病理积分差异无统计学意义（P＞0．05）。慢性支气管炎组NF-κB、MHC I、CD8＋T细胞、VEGF表达的中位数（4．84、2．48、5．35、5．02）较假吸烟组（1．18、1．25、1．33、1．18）、NAC组（2．18、1．46、2．35、2．02）明显升高（P ＜0．05），而假吸烟组与NAC组的差异无统计学意义（P＞0．05）。慢性支气管炎组NF-κB、MHC I与CD8＋T细胞呈正相关（r＝0．670，P＜0．01；r＝0．701，P＜0．01）， CD8＋T细胞与VEGF、小气道病理积分呈正相关（r＝0．689，r＝0．782）。结论 NAC可能通过抑制小气道上皮组织生成NF-κB、MHC I来减轻CD8＋T细胞和VEGF的表达从而减轻小气道炎症。
목적： CD8＋T세포재만성조새성폐질병환자기도중증다차지속존재，관찰CD8＋T세포재연초연무폭로급지다당（ lipopolysaccharide ， LPS）유도대서만성지기관염적막성지기관표체이탐토CD8＋T세포재만성지기관염중적작용。방법18지건강웅성Wistar대서안수궤수자표법분위3조：가흡연조、만성지기관염조、N-을선반광안산（ acetylcysteine ， NAC）조，가흡연조경기도주입등삼염수，만성지기관염대서모형채용2차기관내주입LPS급연훈4주법제비，NAC조재만성지기관염조기출상여NAC（200 mg／kg）관위간예。각조대서취폐조직HE염색관찰막성지기관적병리형태병진행염증병변병리평분，핵인자-κB（nuclear factorκB， NF-κB）、Ⅰ류주요상용성복합체（major histocompatibility complex class I ， MHC I）、CD8＋T세포화혈관내피생장인자（vascular endothelial growth factor ， VEGF）면역조화채용면역조화SP법염색검측。결과가흡연조、NAC조병리적분[1．17±2．40、4．66±2．25]균교만성지기관염조（10．83±3．31）명현강저（P ＜0．05），가흡연조여NAC조병리적분차이무통계학의의（P＞0．05）。만성지기관염조NF-κB、MHC I、CD8＋T세포、VEGF표체적중위수（4．84、2．48、5．35、5．02）교가흡연조（1．18、1．25、1．33、1．18）、NAC조（2．18、1．46、2．35、2．02）명현승고（P ＜0．05），이가흡연조여NAC조적차이무통계학의의（P＞0．05）。만성지기관염조NF-κB、MHC I여CD8＋T세포정정상관（r＝0．670，P＜0．01；r＝0．701，P＜0．01）， CD8＋T세포여VEGF、소기도병리적분정정상관（r＝0．689，r＝0．782）。결론 NAC가능통과억제소기도상피조직생성NF-κB、MHC I래감경CD8＋T세포화VEGF적표체종이감경소기도염증。
Objective CD8 +T cells increased in the airway of patients with chronic obstructive pulmonary disease and exis -ted constantly .The aim was to investigate the role of CD 8 +T-cells in rats with chronic bronchitis ( CB) which was induced by cigarette smoking and intratracheal injection with lipopolysaccharide ( LPS) . Methods 18 health Wistar rats were radomly divided into sham smoking group(group A), CB group(group B) and N-acetylcysteine prevention group (group C).The rats in group B and group C re-ceived intratracheal injection with LPS twice and exposed to cigarette smoking for 4 weeks to induce CB model .The rats in Group C re-ceiving intragastric administration with N-acetylcysteine (NAC)(200mg/kg) before received LPS and smoking.Group A was the sham smoking group.The lung tissue of all rats were stained by HE then evaluated about pathological scores .The expression of nuclear fac-tor-κB (NF-κB), major histocompatibility complex class I (MHCI), CD8 +T cell and Vascular endothelial growth factor (VEGF) in airway were detected by immunohistochemisty which was stained by labeled streptavidin biotin method . Results The pathological scores of airway ( 10 .83 ±3 .31 ) in group B were higher than (1.17 ±2.40) in group A(P <0.05).The pathological scores of airway(4.66 ±2.25) in group C were less than (10.83 ±3.31) in group B(P <0.05).The expression of NF-κB(4.84), MHC I (2.48),CD8 +T cell(5.35)and VEGF(5.02) in airway increased in group B when compared with (1.18, 1.25, 1.33) and (1.18) in group A respectively(P <0.05).The expression of NF-κB (2.18), MHC I(1.46),CD8 +(2.35)and VEGF(2.02) in airway decreased in group C when compared with (4.84), MHC I(2.48),CD8 +T cell(5.35)and VEGF(5.02) in group B respectively (P<0.05 ). There were positive correlations between the expression of NF-κB, MHC I and CD8 +T cells in airways(r=0.670, r=0.701, respec-tively, all P<0.01).There were positive correlations between the expression of CD 8 +T cells and VEGF the pathological scores of air-ways(r=0.689, r=0.782, respectively, all P<0.01). Conclusion NAC can inhibit airway inflammation which is regulated by CD8 +T-cells and VEGF through suppressing the expression of NF -κB and MHC I.