CAJ | 학술논문

目的：研究脂多糖（ LPS）诱导的脓毒症性急性肾损伤（ AKI）小鼠Toll 样受体2（TLR2）的表达规律、分布特点并对其机制进行初步探讨。方法采用小鼠腹腔注射LPS造成脓毒症性AKI模型，将40只清洁级小鼠随机分为生理盐水（NS）对照组（20只）和LPS模型组（20只），分别测定各组血清尿素氮、肌酐及24 h尿蛋白水平，HE染色观察肾组织病理变化。应用免疫组化染色法观察TLR2在两组肾脏的分布特点。应用实时荧光定量PCR（ real－time quantitative PCR）法检测两组肾组织TLR2 mRNA的表达水平。结果腹腔注射LPS后24 h血清尿素氮、肌酐及24 h尿蛋白水平较对照组明显升高，肾脏病理变化亦支持AKI模型造模成功。应用免疫组化染色法检测TLR2在NS组小鼠肾小球内皮细胞有少量表达，足细胞几乎无表达，而在LPS组肾小球内皮细胞及足细胞表达明显增多，而且实时定量PCR法显示，LPS组肾组织TLR2 mRNA表达较NS组明显增高（5．52±0．21 vs 1．00±0．05，P＜0．01）。结论在LPS诱导的脓毒症性AKI中，肾组织TLR2表达明显上调，尤其足细胞及肾小球内皮细胞表达明显增加。 TLR2信号途径在足细胞和肾小球内皮细胞的激活可能介导脓毒症性AKI的发生。
목적：연구지다당（ LPS）유도적농독증성급성신손상（ AKI）소서Toll 양수체2（TLR2）적표체규률、분포특점병대기궤제진행초보탐토。방법채용소서복강주사LPS조성농독증성AKI모형，장40지청길급소서수궤분위생리염수（NS）대조조（20지）화LPS모형조（20지），분별측정각조혈청뇨소담、기항급24 h뇨단백수평，HE염색관찰신조직병리변화。응용면역조화염색법관찰TLR2재량조신장적분포특점。응용실시형광정량PCR（ real－time quantitative PCR）법검측량조신조직TLR2 mRNA적표체수평。결과복강주사LPS후24 h혈청뇨소담、기항급24 h뇨단백수평교대조조명현승고，신장병리변화역지지AKI모형조모성공。응용면역조화염색법검측TLR2재NS조소서신소구내피세포유소량표체，족세포궤호무표체，이재LPS조신소구내피세포급족세포표체명현증다，이차실시정량PCR법현시，LPS조신조직TLR2 mRNA표체교NS조명현증고（5．52±0．21 vs 1．00±0．05，P＜0．01）。결론재LPS유도적농독증성AKI중，신조직TLR2표체명현상조，우기족세포급신소구내피세포표체명현증가。 TLR2신호도경재족세포화신소구내피세포적격활가능개도농독증성AKI적발생。
Objective To investigate the expression of Toll -like receptor 2 ( TLR2 ) in the lipopolysaccharide ( LPS ) -induced septic acute kidney injury ( AKI ) mice and the potential mechanism.Methods Using LPS-treated mice as a model of septic AKI , forty mice were randomly divided into normal control group (n=20), LPS group (n=20).Urinary albumin levels of 24 hours, blood urea nitrogen and creatinine were tested .The expression and distribution of TLR 2 in kidney were determined by immunohistochemistry .Reverse transcriptional -polymerase chain reaction ( RT-PCR ) was performed to evaluate the mRNA levels of TLR 2.Results In the LPS -treated mice, urinary albumin levels increased associated with the elevation of blood urea nitrogen and creatinine levels , indicating the successful induction of septic AKI .Compared with the control group , the expression of TLR2 in podocytes and glomerular endothelial cells of kidney significantly increased in LPS group .TLR2 mRNA expression was up -regulated in LPS group compared with the control group (5.52 ±0.21 vs 1.00 ±0.05, P <0.01).Conclusion LPS treatment led to an significant increase of TLR2 expression , especially in the podocytes and glomerular endothelial cells of kidney .The activation of TLR2 signal way might play an important role in the pathogenesis of septic AKI .