CAJ | 학술논문

目的：基于对TLR9－MyD88－NF－κB通路的干预作用，阐明解毒祛瘀滋肾方对狼疮鼠肾脏的保护作用。方法将30只MRL／lpr狼疮鼠随机分为模型对照组、泼尼松治疗组、中药组共3组，对各治疗组进行相应的药物治疗，疗程8周。采用HE染色法、PAS染色法、Masson染色法分别对MRL／lpr小鼠肾脏切片进行病理染色，观察比较3组小鼠病理变化及治疗效果；采用real－time PCR法观察比较各组小鼠TLR－9、MyD88、NF－κB mRNA表达量的差异。结果与模型组比较，中药组能明显改善MRL／lpr小鼠的肾组织病理损伤。 Real－time PCR法结果显示：中药组MRL／lpr小鼠的肾组织TLR－9、MyD88、NF－κB mRNA表达均低于模型组（均为P＜0．05）。结论解毒祛瘀滋肾方对MRL／lpr小鼠肾脏具有保护作用，可对其病理变化产生影响，减轻其肾脏损害，延缓病程，并与解毒祛瘀滋肾方对MRL／lpr小鼠TLR－9－MyD88－NF－κB信号通路的抑制作用相关。
목적：기우대TLR9－MyD88－NF－κB통로적간예작용，천명해독거어자신방대랑창서신장적보호작용。방법장30지MRL／lpr랑창서수궤분위모형대조조、발니송치료조、중약조공3조，대각치료조진행상응적약물치료，료정8주。채용HE염색법、PAS염색법、Masson염색법분별대MRL／lpr소서신장절편진행병리염색，관찰비교3조소서병리변화급치료효과；채용real－time PCR법관찰비교각조소서TLR－9、MyD88、NF－κB mRNA표체량적차이。결과여모형조비교，중약조능명현개선MRL／lpr소서적신조직병리손상。 Real－time PCR법결과현시：중약조MRL／lpr소서적신조직TLR－9、MyD88、NF－κB mRNA표체균저우모형조（균위P＜0．05）。결론해독거어자신방대MRL／lpr소서신장구유보호작용，가대기병리변화산생영향，감경기신장손해，연완병정，병여해독거어자신방대MRL／lpr소서TLR－9－MyD88－NF－κB신호통로적억제작용상관。
ObjectiveToclarifytheprotectiveactionofaChinesemedicine,Jie-Du-Qu-Yu-Zi-Shen prescription, on the lupus nephritis in MRL/lpr mice through the TLR9-MyD88-NF-κB signaling pathway .Methods Thirty MRL/lpr mice were randomly divided into model group , prednisone group , and traditional Chinese medicine ( TCM) group (n=10).Each treatment group received appropriate treatment or drug therapy for 8 weeks.The pathological changes of mouse renal tissues in the three groups were examined and compared using HE , PAS, and Masson staining .Real-time PCR was performed to compare the expression of TLR-9, MyD88, NF-κBm RNA mRNA in each group of the mice . Results Compared with the model group , the Chinese medicine Jie-Du-Qu-Yu-Zi-Shen prescription significantly improved the renal pathological tissue damages in the MRL/lpr mice.Real-time PCR assay showed that the expression levels of TLR-9, MyD88, NF-κB mRNA in the TCM group were significantly lowered (P<0.01 for all).The differences between the TCM group and prednisone group were statistically not significant ( P >0.05 ) .Conclusions Jie-Du-Qu-Yu-Zi-Shen prescription has protective effect on the kidney of MRL /lpr mice, alleviating its pathological changes , and delaying the disease course, probably, through inhibiting the TLR-9-MyD88-NF-κB signaling pathway in the kidneys of MRL/lpr mice.