CAJ | 학술논문

目的探讨MRL/lpr狼疮鼠模型中重要的抗氧化因子γ-谷氨酰半胱氨酸合成酶(γ-GCS)在肾纤维化发生过程所起的作用.方法应用半定量反转录聚合酶链反应(RT-PCR)和免疫组织化学技术,观察MRL/lpr狼疮鼠及正常对照组小鼠肾组织中结缔组织生长因子(CTGF)和γ-GCS的表达,并进一步分析γ-GCS表达量与CTGF之间存在的内在联系.结果 MRL/lpr小鼠模型肾脏CTGF mRNA转录及蛋白表达均较正常小鼠显著增加(CTGF mRNA:1.052±0.004和0.402±0.009,P<0.01;CTGF蛋白:3.364±0.460和1.206±0.271,P<0.01);而γ-GCS mRNA表达较健康对照组显著减少(0.952±0.011和1.145±0.066,P<0.01);Pearson回归分析显示MRL/lpr狼疮小鼠肾组织中CTGF mRNA表达量与γ-GCS mRNA表达量量负相关(r=-0.902,P<0.01).结论 MRL/lpr小鼠肾脏中存在γ-GCS表达异常降低,机体抗氧化能力减低,而且与CTGF的表达呈负相关,可能因此而参与了肾脏纤维化的进程.
목적 탐토MRL/lpr랑창서모형중중요적항양화인자γ-곡안선반광안산합성매(γ-GCS)재신섬유화발생과정소기적작용.방법 응용반정량반전록취합매련반응(RT-PCR)화면역조직화학기술,관찰MRL/lpr랑창서급정상대조조소서신조직중결체조직생장인자(CTGF)화γ-GCS적표체,병진일보분석γ-GCS표체량여CTGF지간존재적내재련계.결과 MRL/lpr소서모형신장CTGF mRNA전록급단백표체균교정상소서현저증가(CTGF mRNA:1.052±0.004화0.402±0.009,P<0.01;CTGF단백:3.364±0.460화1.206±0.271,P<0.01);이γ-GCS mRNA표체교건강대조조현저감소(0.952±0.011화1.145±0.066,P<0.01);Pearson회귀분석현시MRL/lpr랑창소서신조직중CTGF mRNA표체량여γ-GCS mRNA표체량량부상관(r=-0.902,P<0.01).결론 MRL/lpr소서신장중존재γ-GCS표체이상강저,궤체항양화능력감저,이차여CTGF적표체정부상관,가능인차이삼여료신장섬유화적진정.
Objective To investigate the effect of γ-glutamylcysteine synthetase (γ-GCS),in the kidney fibrosis of MRL/lpr lupus mice.Methods The expression of connective tissue growth factor(CTGF)and γ-GCS in the kidney tissue of MRL/lpr lupus mice and control mice were detected by reverse transcriptase PCR (RT-PCR)and immunohistochemistry.The relationship between CTGF and γ-GCS was analyzed.Results The transcription and expression of CTGF in the kidney tissue of MRL/lpr lupus mice was significantly higher as compared with that of the control mice(CTGF mRNA:1.052±0.004 vs 0.402±0.009,P<0.01;CTGF protein:3.364±0.460 vs 1.206±0.271,P<0.01);whereas the expression of γ-GCS mRNA was decreased in MRL/lpr lupus mice(0.952±0.011 vs 1.145±0.066,P<0.01).Pearson's regression analysis showed that there was a negative correlation between CTGF and γ-GCS(r=-0.902,P<0.01).Conclusion The decreased expression of γ-GCS in the kidney of MRL/lpr lupus mice may compromise the ability of antioxidative stress,and there is a negative correlation between γ-GCS and CTGF.This suggests that the perturbation of γ-GCS may contribute to the progress of kidney fibrosis.