【摘要】 目的：探讨茶多酚对过敏性鼻炎大鼠过敏性症状的改善作用及其机制。方法：40只SD大鼠随机分为正常组、模型组、茶多酚组和氯雷他定组，每组各10只。除正常组外，其余组大鼠通过卵白蛋白+氢氧化铝粉建立过敏性鼻炎模型大鼠，造模成功后，茶多酚组大鼠灌胃茶多酚混悬液300 mg/kg，氯雷他定组大鼠灌胃氯雷他定0.9 mg/kg，正常组和模型组灌胃等量生理盐水。比较各组大鼠行为学症状评分，检测各组大鼠血清免疫球蛋白（IgE）、组胺（HIS）、白细胞介素（IL）-10和IL-17的含量，利用HE染色技术观察鼻黏膜组织病理损伤，qRT-PCR技术和蛋白印迹技术检测转录因子孤核受体（RORγt）、叉头翼状螺旋转录因子3(Foxp3)以及p38丝裂原活化蛋白激酶（MAPK）mRNA和蛋白表达量。结果：正常组大鼠鼻黏膜组织无明显异常，上皮结构完整，纤毛柱状上皮排列整齐；模型组大鼠鼻黏膜上皮结构紊乱，部分上皮细胞脱落，腺体增生、肿胀，炎性细胞浸润；茶多酚组和氯雷他定组大鼠鼻黏膜病理损伤程度较轻，上皮结构较正常，炎性细胞浸润程度较模型组减少。与正常组比较，模型组大鼠行为症状学评分，IgE、IL-17和HIS水平，ROR γt mRNA和蛋白表达量，p38MAPK mRNA表达量以及p-p38 MAPK蛋白表达量均升高，IL-10水平，Foxp3 mRNA和蛋白表达量均降低，差异均有统计学意义（P<0.001）；与模型组比较，茶多酚组和氯雷他定组大鼠行为症状学评分，IgE、IL-17和HIS水平，ROR γt mRNA和蛋白表达量，p38 MAPK m RNA表达量以及p-p38 MAPK蛋白表达量均降低，IL-10水平，Foxp3 mRNA和蛋白表达量均升高，差异均有统计学意义（P<0.001）。茶多酚显著降低了大鼠的行为学评分，并降低了血清中IgE、HIS、IL-17和IL-10水平，差异均有统计学意义（P<0.001）。鼻黏膜组织病理学观察显示，茶多酚减轻了鼻黏膜上皮结构的紊乱和炎性细胞浸润。此外，茶多酚显著下调了ROR γt和p38 MAPK m RNA及蛋白的表达，同时上调了Foxp3 mRNA及蛋白的表达，差异均有统计学意义（P<0.05）。结论：茶多酚可减轻过敏性鼻炎大鼠鼻部过敏症状，其可能是通过抑制p38 MAPK信号通路调节Treg/Th17细胞免疫平衡发挥作用。更多还原

【Abstract】 Objective: To investigate the improvement effect and its mechanism of green tea polyphenols on allergic rhinitis inrats. Methods: Forty rats were randomly divided into normal group, model group, green tea polyphenol group and loratadine group,with 10 rats in each group. Except for normal group, allergic rhinitis rats in other groups were infected by obumin+aluminumhydroxide powder. After successful model creation, green tea polyphenol group rats were intragastatically injected with green teapolyphenol suspension 300 mg/kg, loratadine group rats were intragastatically injected with loratadine 0.9 mg/kg, normal group andmodel group were intragastatically injected with the same amount of normal saline. Behavioral symptom scores, serumimmunoglobulin E(IgE), histamine(HIS), interleukin(IL)-10 and IL-17 were compared among all groups, and pathological injuryof nasal mucosa was observed by HE staining. q RT-PCR and western blot were used to detect m RNA and protein expression levelsof retinoic acid receptor-related orphan receptor gamma-t(RORγt), forkhead box P3(Foxp3) and p38 mitogen-activated proteinkinase(MAPK). Results: In normal group, there was no obvious abnormality in nasal mucosa, and the epithelium structure wasintact and arranged neatly. In the model group, the nasal mucosal epithelium was disorganized, some epithelial cells were shed,glands were hyperplastic and swollen, and inflammatory cells were infiltrated. In the green tea polyphenol group and loratadinegroup, the pathological damage of nasal mucosa was reduced, the epithelial structure was slightly normal, and the inflammatorycells were reduced. Compared with the normal group, behavioral symptomatology scores, IgE, IL-17 and HIS levels, ROR γt mRNA and protein expression, p38 MAPK mRNA expressionand p-p38 MAPK protein expression of rats in the modelgroup were increased; while IL-10 level, the m RNA and protein expressions of Foxp3 were decreased, with statistically significant differences(P<0.05). Compared with the model group,the behavioral symptomatology scores, Ig E, IL-17 and HIS levels, ROR γt m RNA and protein expression levels, p38 MAPKm RNA expression levels and p-p38 MAPK protein expression levels of green tea polyphenol group and loratadine group weredecreased, while IL-10 levels, m RNA and protein expressions of Foxp3 were increased, with statistically significant differences(P<0.05). Green tea polyphenols significantly reduced behavioral scores in rats and decreased serum levels of Ig E, HIS, IL-17,and IL-10, with statistically significant differences(P<0.05). Histopathological examination of nasal mucosal tissue revealed thatgreen tea polyphenols mitigated disruption of the nasal epithelial structure and inflammatory cell infiltration. Furthermore, teapolyphenols significantly downregulated RORγt and p38 MAPK m RNA and protein expression while simultaneously upregulatingFoxp3 m RNA and protein expression, with statistically significant differences(P<0.05). Conclusion: Green tea polyphenols canimprove the nasal allergic symptoms of rats with allergic rhinitis, which may play a role in regulating the immune balance of Treg/Th17 cells by inhibiting p38 MAPK pathway.更多还原