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目的:探讨蛋白激酶C(PKC)和激活蛋白-1(AP-1)信号转导级联在变应性鼻炎(AR)患者外周血T淋巴细胞IL-5表达中的作用。方法:25例AR患者和23例鼻中隔偏曲(DNS)患者为研究对象,分别从每位受试者外周血中分离T淋巴细胞,并随机分为空白组、PKC激动剂12-肉豆蔻酰-13-乙酸佛波酯(PMA)组、PMA和AP-1抑制剂姜黄素组进行培养。将培养的T淋巴细胞涂片,用免疫细胞化学染色方法检测AP-1的表达,用酶联免疫吸附(ELISA)法检测上清液中的IL-5含量。结果:①加PMAAR组T淋巴细胞的AP-1活化细胞百分比和培养上清液中的IL-5与DNS空白组与AR空白组比较,均差异有统计学意义(均P<0.01);与加PMADNS组及加PMA和姜黄素DNS组T淋巴细胞比较,均差异有统计学意义(均P<0.01);与加PMA和姜黄素AR组T淋巴细胞比较,差异亦有统计学意义(P<0.01);②加PMA和姜黄素AR组T淋巴细胞AP-1活化细胞百分比、培养上清液中的IL-5含量与AR空白组、加PMAAR组、DNS空白组、加PMADNS组、加PMA和姜黄素DNS组比较,均差异有统计学意义(均P<0.01);③T淋巴细胞的AP-1活化与IL-5表达呈显著正相关(r=0.92,P<0.01)。结论:AR患者T淋巴细胞PKC活化后促进IL-5表达增加的生物信号可能是通过AP-1进行转导,提示T淋巴细胞PKC-AP-1信号转导级联的激活可能是AR发病机制之一。
Objective: To investigate the role of protein kinase C (PKC) and activator protein-1 (IL-1) signaling cascades in the expression of IL-5 in peripheral blood T lymphocytes of patients with allergic rhinitis (AR). Methods: Twenty-five patients with AR and 23 patients with nasal septum deviation (DNS) were divided into T lymphocytes from peripheral blood of each subject and randomly divided into blank group, PKC agonist 12-myristoyl -13-phorbol acetate (PMA) group, PMA and the AP-1 inhibitor curcumin group. The cultured T lymphocytes were smeared and the expression of AP-1 was detected by immunocytochemical staining. The content of IL-5 in the supernatant was detected by enzyme-linked immunosorbent assay (ELISA). Results: ①The percentage of AP-1 activated cells in T lymphocytes plus PMAAR group was significantly lower than that in AR blank group (P <0.01) Compared with T-lymphocytes in PMADNS group and PMA plus curcumin group, there was significant difference (all P <0.01); compared with T cells in PMA group and curcumin group, the differences were also statistically significant (P <0.01). (2) The percentage of AP-1 activated cells in T lymphocytes of PMA group and curcumin AR group was significantly higher than that in AR blank group, PMAAR group, DNS blank group and PMADNS group PMA and curcumin DNS group, the difference was statistically significant (all P <0.01); ③T-lymphocyte AP-1 activation and IL-5 expression was positively correlated (r = 0.92, P <0.01). CONCLUSION: The biological signals that promote the expression of IL-5 after PKC activation of T lymphocytes in AR patients may be transduced by AP-1, suggesting that the activation of PKC-AP-1 signal transduction cascade in T lymphocytes may be the pathogenesis of AR one.