CAJ | 학술논문

目的：探讨 Toll 样受体2(TLR2)介导的 c-Jun 氨基末端激酶(JNK)信号分子参与小鼠支气管哮喘发病的作用机制。方法健康 SPF 级 C57(TLR2野生型)鼠和 TLR2基因缺失(TLR2-/-)鼠各14只,按随机数字表法分为4组：C57对照组、C57哮喘组、TLR2-/-对照组、TLR2-/-哮喘组,每组7只,哮喘组以卵清蛋白(OVA)腹腔注射联合雾化吸入致敏和激发建立哮喘模型,对照组以生理盐水代替 OVA致敏和激发。利用免疫组织化学染色技术( ABC 法)检测TLR2蛋白在 C57对照组、C57哮喘组肺内的表达差异,JNK及磷酸化 JNK(P-JNK)蛋白表达在各组肺内的表达差异。结果 HE 染色提示较其余3组,C57哮喘组有较明显的炎症细胞浸润及呼吸道平滑肌增生。以平均吸光度(mA)衡量各组织蛋白相对表达量,免疫组化结果提示 TLR2蛋白在C57哮喘组表达显著高于 C57对照组(P <0．01),JNK 蛋白在各组的表达差异无统计学意义,P-JNK 蛋白在 C57哮喘组肺组织的表达量显著高于 C57对照组、TLR2-/-哮喘组、TLR2-/-对照组(F =43．261,P <0．01)。结论 TLR2介导的 JNK 信号分子通路可能参与了支气管哮喘的发病过程。
목적：탐토 Toll 양수체2(TLR2)개도적 c-Jun 안기말단격매(JNK)신호분자삼여소서지기관효천발병적작용궤제。방법건강 SPF 급 C57(TLR2야생형)서화 TLR2기인결실(TLR2-/-)서각14지,안수궤수자표법분위4조：C57대조조、C57효천조、TLR2-/-대조조、TLR2-/-효천조,매조7지,효천조이란청단백(OVA)복강주사연합무화흡입치민화격발건립효천모형,대조조이생리염수대체 OVA치민화격발。이용면역조직화학염색기술( ABC 법)검측TLR2단백재 C57대조조、C57효천조폐내적표체차이,JNK급린산화 JNK(P-JNK)단백표체재각조폐내적표체차이。결과 HE 염색제시교기여3조,C57효천조유교명현적염증세포침윤급호흡도평활기증생。이평균흡광도(mA)형량각조직단백상대표체량,면역조화결과제시 TLR2단백재C57효천조표체현저고우 C57대조조(P <0．01),JNK 단백재각조적표체차이무통계학의의,P-JNK 단백재 C57효천조폐조직적표체량현저고우 C57대조조、TLR2-/-효천조、TLR2-/-대조조(F =43．261,P <0．01)。결론 TLR2개도적 JNK 신호분자통로가능삼여료지기관효천적발병과정。
Objective To explore the mechanism of c-Jun N-terminal kinase mediated by Toll like receptor 2 in murine asthma. Methods 14 healthy SPF grade C57 wild-type mice and 14 TLR2 knockout (TLR2 - / - ) mice were randomly divided into four groups: C57 control group, C57 asthma group, TLR2 - / - control group, TLR2 - / - asth-ma group (n = 7). We utilized intraperitoneal injection combined with inhalation of ovalbumin (OVA) to sensitize and challenge the mice, thus establishing the experimental models of asthma. Meanwhile, the control group received normal saline instead of OVA. The protein expression of TLR2 was detected by immunohistochemistry(ABC meth-od) in C57 control group and C57 asthma group,as well as JNK and phosphorylation c-Jun(P-JNK) between each group. Results In C57 asthma group,HE-staining showed more obvious inflammatory cell infiltration around bron-chi and airway smooth muscle hyperplasia than the other three groups. The relative protein expressions were meas-ured by mean absorbance(mA). Immunohistochemistry indicated that mean absorbance values of TLR2 was signifi-cantly higher in C57 asthma group than those of C57 control group (P < 0. 01). There was no obvious difference of JNK protein expression between each group. The immunoexpression of P-JNK in C57 asthma group was notablely higher than those of C57 control group, TLR2 - / - asthma group, TLR2 - / - control group (F = 43. 261,P < 0. 01). Conclusion TLR2-mediated JNK signaling molecules may be involved in the process of murine asthma.