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目的:对细胞黏附分子(CAM)及一氧化氮合酶(NOS)进行原位观察,探讨它们在变应性鼻炎(AR)发病中的作用。方法:采用链霉卵白素-生物素复合体(SABC)法,对AR患者及对照组手术切除的下鼻甲黏膜内细胞间黏附分子-1(ICAM-1)、血管CAM-1(VCAM-1)和淋巴细胞功能相关抗原-1(LFA-1),以及神经型NOS(nNOS)、诱导型NOS(iNOS)和内皮细胞型NOS(eNOS)进行原位检测。结果:AR下鼻甲黏膜内3种CAM表达的阳性细胞数ICAM-1为[(14.4±2.2)个/HP(×400),以下同],LFA-1为(17.2±3.3)个/HP,VCAM-1为(11.5±2.7)个/HP;对照组下鼻甲黏膜内3种CAM表达的阳性细胞数ICAM-1为(8.7±1.8)个/HP,LFA-1为(10.3±2.1)个/HP,VCAM-1为(6.9±1.8)个/HP。t值分别是11.57,10.02和8.07(均P<0.01)。AR及对照组下鼻甲黏膜内nNOS表达的阳性细胞数分别为(9.4±1.7)个/HP和(4.7±1.3)个/HP,t值为12.62,(P<0.01);iNOS表达的阳性细胞数分别为(27.5±3.2)个/HP和(4.3±1.7)个/HP,t值为36.03(P<0.01)。eNOS表达的阳性细胞数分别为(6.5±2.1)个/HP,(6.2±1.9)个/HP,t值为0.62(P>0.05)。结论:CAM在黏膜上皮、腺上皮、血管内皮以及黏膜下的各种炎性细胞等的表达,说明CAM参与AR的发生、发展。nNOS和iNOS在AR的发病过程中可能起重要作用。
Objective: To observe in situ cell adhesion molecule (CAM) and nitric oxide synthase (NOS) and their roles in the pathogenesis of allergic rhinitis (AR). Methods: The expressions of intercellular adhesion molecule-1 (ICAM-1), vascular endothelial cell CAM-1 (VCAM-1) in the inferior turbinate mucosa of AR patients and control group were detected by streptavidin-biotin complex ) And lymphocyte function associated antigen-1 (LFA-1), as well as neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial cell NOS (eNOS). Results: The number of ICAM-1 positive cells in AR of inferior turbinate mucosa was (14.4 ± 2.2) / HP (× 400), the same below], LFA-1 was (17.2 ± 3.3) / HP, (11.5 ± 2.7) / HP for VCAM-1, ICAM-1 was (8.7 ± 1.8) / HP and (10.3 ± 2.1) LAC-1 was positive for the three CAMs in the inferior turbinate mucosa / HP, VCAM-1 was (6.9 ± 1.8) / HP. The t values were 11.57, 10.02 and 8.07 (all P <0.01). The positive number of nNOS expression in inferior turbinate mucosa of AR and control group were (9.4 ± 1.7) / HP and (4.7 ± 1.3) / HP respectively, t = 12.62, (P <0.01) The numbers were (27.5 ± 3.2) / HP and (4.3 ± 1.7) / HP respectively, with a t value of 36.03 (P <0.01). The number of positive cells in eNOS expression was (6.5 ± 2.1) /HP, (6.2 ± 1.9) / HP, respectively, with a t value of 0.62 (P> 0.05). CONCLUSION: The expression of CAM in mucosal epithelium, glandular epithelium, vascular endothelium and submucosal inflammatory cells indicates that CAM participates in the occurrence and development of AR. nNOS and iNOS may play an important role in the pathogenesis of AR.