CAJ | 학술논문

目的：观察雷公藤甲素对哮喘小鼠IL－23、Th17细胞及其细胞因子IL－17表达的情况，探讨其对Th17细胞介导的哮喘气道炎症的影响及其作用机制，为雷公藤甲素治疗哮喘提供作用靶点。方法：SPF 级BALB／c 小鼠32只，随机分为正常组（NC 组）、哮喘组（A 组）、哮喘雷公藤甲素干预组（TA 组）和哮喘地塞米松干预组（DA 组），每组8只。哮喘组以卵白蛋白和氢氧化铝致敏；卵白蛋白滴鼻吸入激发。雷公藤甲素干预组及地塞米松干预组致敏及激发方法均同哮喘组，这两组在每次激发前30 min 分别予腹腔注射雷公藤甲素及地塞米松，正常对照组致敏与激发均以生理盐水代替。细胞计数器计算肺泡灌洗液（BALF）中白细胞总数及嗜酸性粒细胞的数目；酶联免疫吸附试验（ELISA）检测小鼠BALF IL－23，IL－17的含量；HE染色观察小鼠肺组织病理变化；免疫组化法检测肺组织IL－17蛋白表达水平；qRT－PCR 检测右肺组织中IL－17mRNA 的表达；流式细胞仪检测外周血Th17细胞占CD4＋ T 淋巴细胞百分率。结果：哮喘组肺泡灌洗液（BALF）中白细胞（WBC）、嗜酸性粒细胞（Eos）、IL－23、IL－17的含量、肺组织中IL－17蛋白及IL－17 mRNA 表达、外周血Th17细胞占CD4＋T 细胞的比率均高于对照组（P＜0．05），雷公藤甲素干预组和地塞米松干预组中上述各指标低于哮喘组（P＜0．05）；雷公藤甲素干预组与地塞米松干预组上述各指标间差异无显著性（P＞0．05）。结论：雷公藤甲素可抑制哮喘气道炎症，其作用机制可能通过抑制IL－23／Th17（IL－17）炎症轴实现。
목적：관찰뢰공등갑소대효천소서IL－23、Th17세포급기세포인자IL－17표체적정황，탐토기대Th17세포개도적효천기도염증적영향급기작용궤제，위뢰공등갑소치료효천제공작용파점。방법：SPF 급BALB／c 소서32지，수궤분위정상조（NC 조）、효천조（A 조）、효천뢰공등갑소간예조（TA 조）화효천지새미송간예조（DA 조），매조8지。효천조이란백단백화경양화려치민；란백단백적비흡입격발。뢰공등갑소간예조급지새미송간예조치민급격발방법균동효천조，저량조재매차격발전30 min 분별여복강주사뢰공등갑소급지새미송，정상대조조치민여격발균이생리염수대체。세포계수기계산폐포관세액（BALF）중백세포총수급기산성립세포적수목；매련면역흡부시험（ELISA）검측소서BALF IL－23，IL－17적함량；HE염색관찰소서폐조직병리변화；면역조화법검측폐조직IL－17단백표체수평；qRT－PCR 검측우폐조직중IL－17mRNA 적표체；류식세포의검측외주혈Th17세포점CD4＋ T 림파세포백분솔。결과：효천조폐포관세액（BALF）중백세포（WBC）、기산성립세포（Eos）、IL－23、IL－17적함량、폐조직중IL－17단백급IL－17 mRNA 표체、외주혈Th17세포점CD4＋T 세포적비솔균고우대조조（P＜0．05），뢰공등갑소간예조화지새미송간예조중상술각지표저우효천조（P＜0．05）；뢰공등갑소간예조여지새미송간예조상술각지표간차이무현저성（P＞0．05）。결론：뢰공등갑소가억제효천기도염증，기작용궤제가능통과억제IL－23／Th17（IL－17）염증축실현。
Objective:To observe the effect of triptolide on asthmatic mice IL-23, Th17 cells and their cytokine IL-17 expression,and to explore its effect on Th17 cell-mediated airway inflammation,and its mechanism of action,which provides targets for triptolide in treatment of asthma.Methods: 32 SPF level BALB/c mice were randomly divided into normal control group ( NC ) , asthmatic group ( A ) , triptolide group ( TA group ) and dexamethasone group ( DA group ) , n=8.Asthmatic group with ovalbumin sensitization and aluminum hydroxide;ovalbumin intranasal inhalation challernge.Mice of triptolide group and dexamethasone group were sensitized and challenged as asthmatic group, and the two groups were respectively given triptolide and dexamethasone by intraperitoneal injection 30 minutes before challenged.Mice of control group was sensitized and challenged by saline.The total number of white blood cells and the number of eosinophils of BALF were calculated by cell counter.IL-23 and IL-17 levels in BALF were measured by ELISA.Lung tissue were stained with hematoxyin and eosin(HE).IL-17 protein expression levels were detected by immu-nohistochemistry in lung tissue,and the mRNA expression levels of right lung tissue were detected by qRT-PCR.Th17 percentage of CD4+T lymphocytes were analyzed by flow cytometry.Results:Numbers of white blood cells( WBC) and eosinophils( Eos) of BALF, IL-23 and IL-17 levels of BALF,IL-17 protein and IL-17 mRNA expression in lung tissue,and Th17 cell frequencies in peripheral blood were all significantly increased in the asthmatic group compared to the control group(P<0.05),but reduced significantly in triptolide group and dexamethasone group compared to asthmatic group;there was no significant difference in the above mentioned indicators between in triptolide group and dexamethasone group ( P>0.05 ) .Conclusion: Triptolide can inhibit airway inflammation, which mechanism is possible by inhibiting IL-23/Th17(IL-17) inflammatory axis.