【摘要】 目的 :观察吸烟对大鼠肺组织iNOS、eNOSmRNA和蛋白表达以及支气管肺泡灌洗液 (BALF)中NO的影响 ,探讨不同类型的NOS在吸烟所致慢性气道炎症中的作用。方法 :选用Wistar大鼠 80只随机分为对照组 ,被动吸烟组 ,iNOS抑制剂L -NIL干预组及NOS抑制剂L -NAME干预组。用免疫组化法检测iNOS及eNOS的蛋白表达 ,用RT -PCR检测iNOS及eNOSmRNA的表达 ,用Griess法测定BALF中的NO-2 /NO-3 含量。结果 :吸烟大鼠肺组织中iNOSmRNA及其蛋白表达增加 ,eNOSmRNA及蛋白表达下降 ,BALF中细胞总数及NO-2 /NO-3 显著增加 (P <0 0 5 )。在体实验发现 ,L -NIL使BALF中细胞总数及NO-2 /NO-3 下降 (P <0 0 5 ) ;L -NAME对BALF中细胞总数及NO-2 /NO-3 无显著影响 (P >0 0 5 )。结论 :吸烟大鼠肺组织iNOSmRNA和蛋白表达增加 ,eNOSmRNA和蛋白表达减少。活化的iNOS产生大量NO促进炎症发展更多还原

【Abstract】 AIM: To observe the changes of iNOS and eNOS in lung tissue and NO in bronchoalveolar lavage fluid (BALF) in smoking rats. METHODS: 80 Wistar rats were divided into control, smoking group, L-NIL group and L-NAME group (rats were exposed to smoke and injected (i.p.) with selective iNOS inhibitor L-NIL or NOS inhibitor L-NAME). iNOS and eNOS protein levels in whole lung were detected by immunohistochemical staining, and NOS mRNA was quantified using RT-PCR. In addition, NO - 2/NO - 3 was determined using Griess assay. RESULTS: The expression of iNOS mRNA and protein in smoking rats increased, the expression of eNOS mRNA and eNOS protein decreased, and the total cell count and the level of NO - 2/NO - 3in BALF increased( P< 0.05). In vivo , L-NIL reduced the total cell count and NO - 2/NO - 3 in BALF ( P< 0.05), while L-NAME had no effect on them. CONCLUSION: Cigarette smoke increased expression of iNOS mRNA and protein and decreased expression of eNOS mRNA and protein. The large amount of NO generated by iNOS may amplify inflammation in lung tissue.更多还原