CAJ | 학술논문

目的：探讨芪蓟多糖通过 NF -κB 信号通路对大鼠肾小球系膜细胞的影响。方法体外培养大鼠肾小球系膜细胞，用血管紧张素Ⅱ（AngⅡ）刺激系膜细胞增生，分别给予氯沙坦和芪蓟多糖，用酶联免疫吸附法（ELISA）检测肾小球系膜细胞上清液转化生长因子β活化激酶1（TAK1）、肿瘤坏死因子受体相关因子6（TRAF6）、核因子（NF -κB）和纤维粘连蛋白（FN）表达；实时定量 PCR 法检测 TAK1、NF -κB 的表达。结果 ELISA 法对 OD 值的测定，与正常组比较，模型组、芪蓟肾康方多糖高剂量组和低剂量组、氯沙坦组大鼠肾小球系膜细胞中 TAK1、TRAF6、NF -κB 和 FN 表达均升高且有明显差异（P ﹤0.05，P ﹤0.01）；与模型组比较，芪蓟肾康方多糖高剂量组和低剂量组、氯沙坦组可降低 NF -κB 信号转导中各靶点 TAK1、TRAF6、NF -κB 及 FN 的表达，且有明显差异（P ﹤0.01）。实时定量 PCR 法检测，与正常组比较，模型组及芪蓟肾康方多糖高剂量组和低剂量组大鼠肾小球系膜细胞中 TAK1、NF -κB 表达升高，且有明显差异（P ﹤0.05）；与模型组比较，芪蓟肾康方多糖高剂量组和低剂量组大鼠肾小球系膜细胞中 TAK1、NF -κB 明显降低（P ﹤0.05）。在 NF -κB 表达中，芪蓟肾康方多糖高剂量组和低剂量组组间比较无明显差异（P ﹥0.05）。结论芪蓟多糖可能通过下调肾小球系膜细胞 NF -κB mRNA 及 TAK1、TRAF6、NF -κB 和 FN 蛋白表达的水平，抑制核因子信号转导通路的兴奋性，缓解 NF -κB 的释放，减少 FN 的过度表达，从而减轻细胞外基质（ECM）的分泌，降低肾小球的损伤，减缓肾小球的硬化。
목적：탐토기계다당통과 NF -κB 신호통로대대서신소구계막세포적영향。방법체외배양대서신소구계막세포，용혈관긴장소Ⅱ（AngⅡ）자격계막세포증생，분별급여록사탄화기계다당，용매련면역흡부법（ELISA）검측신소구계막세포상청액전화생장인자β활화격매1（TAK1）、종류배사인자수체상관인자6（TRAF6）、핵인자（NF -κB）화섬유점련단백（FN）표체；실시정량 PCR 법검측 TAK1、NF -κB 적표체。결과 ELISA 법대 OD 치적측정，여정상조비교，모형조、기계신강방다당고제량조화저제량조、록사탄조대서신소구계막세포중 TAK1、TRAF6、NF -κB 화 FN 표체균승고차유명현차이（P ﹤0.05，P ﹤0.01）；여모형조비교，기계신강방다당고제량조화저제량조、록사탄조가강저 NF -κB 신호전도중각파점 TAK1、TRAF6、NF -κB 급 FN 적표체，차유명현차이（P ﹤0.01）。실시정량 PCR 법검측，여정상조비교，모형조급기계신강방다당고제량조화저제량조대서신소구계막세포중 TAK1、NF -κB 표체승고，차유명현차이（P ﹤0.05）；여모형조비교，기계신강방다당고제량조화저제량조대서신소구계막세포중 TAK1、NF -κB 명현강저（P ﹤0.05）。재 NF -κB 표체중，기계신강방다당고제량조화저제량조조간비교무명현차이（P ﹥0.05）。결론기계다당가능통과하조신소구계막세포 NF -κB mRNA 급 TAK1、TRAF6、NF -κB 화 FN 단백표체적수평，억제핵인자신호전도통로적흥강성，완해 NF -κB 적석방，감소 FN 적과도표체，종이감경세포외기질（ECM）적분비，강저신소구적손상，감완신소구적경화。
Objective To explore the impacts of Qiji polysaccharose on glomerular mesangial cells via NF - κB signal pathway. Methods The glomerular mesangial cells were cultured in vitro. Ang II was used to stimulate glomerular mesangial cell proliferation. Losartan and Qiji polysaccharose were applied sepa-rately. ELISA was applied to determine the expressions of TAK1,TRAF6,NF - κB and FN in the supernate of glomerular mesangial cells. The real - time quantitative PCR was used to determine the expressions of TAK1 and NF - κB. Results In ELISA determination of OD value,compared with the normal group,the expres-sions of TAK1,TRAF6,NF - κB and FN in glomerular mesangial cells were all increased in the model group, high - dose group and low - dose group of Qiji polysaccharose,as well as Losartan group,indicating the ap-parent differences(P ﹤ 0. 05,P ﹤ 0. 01). Compared with the model group,the expressions of TAK1,TRAF6, NF - κB and FN at each target point of NF - κB transduction were reduced in the high - dose group,low -dose group and Losartan group(P ﹤ 0. 01). In real - time quantitative PCR determination,compared with the normal group,the expressions of TAK1 and NF - κB in glomerular mesangial cells were increased in the mod-el group,high - dose group and low - dose group of Qiji polysaccharose,indicating the obvious difference(P﹤ 0. 05). Compared with the model group,the expressions of TAK1 and NF - κB in glomerular mesangial cells were reduced apparently in the model group,high - dose group and low - dose group of Qiji polysaccharose.Concerning to NF - κB expression,the difference was not significant between the high - dose group and low -dose group of Qiji polysaccharose(P ﹥ 0. 05). Conclusion Qiji polysaccharose inhibits the excitability of nuclear factor signal transduction pathway,relieves NF - κB release,reduces FN over - expression via down- regulating the expressions of TAK1,NF - κB mRNA and the protein expressions of TAK1,TRAF6,NF -κB and FN in glomerular mesangial cells so as to alleviate ECM secretion,reduce glomerular damage and re-tard glomerular sclerosis.