世界科学技术-中医药现代化
世界科學技術-中醫藥現代化
세계과학기술-중의약현대화
WORLD SCIENCE AND TECHNOLOGY-MODERNIZATION OF TRADITIONAL CHINESE MEDICINE
2014年
5期
1156-1161
,共6页
修婵%杨冠琦%赵兴伟%张君
脩嬋%楊冠琦%趙興偉%張君
수선%양관기%조흥위%장군
c-Jun氨基末端激酶%活化蛋白1%纤维粘连蛋白%血管紧张素Ⅱ
c-Jun氨基末耑激酶%活化蛋白1%纖維粘連蛋白%血管緊張素Ⅱ
c-Jun안기말단격매%활화단백1%섬유점련단백%혈관긴장소Ⅱ
c-Jun N-terminal kinase%activator protein-1%fibronectin%Angiotensin II%Qi-Ji Shen-Kang%glomerular mesangial cell
目的：探讨芪蓟肾康方通过JNK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刺激系膜细胞增生，给予芪蓟肾康方黄酮干预，用酶联免疫吸附（ELISA）法检测肾小球系膜细胞上清液 c-Jun 氨基末端激酶（JNK）、活化蛋白1（AP-1）、纤维粘连蛋白（FN）蛋白表达；实时定量 PCR 法检测 JNK、AP-1 mRNA 的表达。结果：与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显升高（P约0.05或 P约0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显降低（P约0.05或 P约0.01）。与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA 表达明显升高（P约0.05或 P约0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA明显降低（P约0.05）。结论：芪蓟肾康方可以通过下调肾小球系膜细胞JNK、AP-1 mRNA及蛋白的表达水平，抑制 JNK 信号转导，降低 AP-1的活性，减少 FN 的增殖，从而减轻 GMC 增生，延缓肾小球的损伤，防止肾小球的硬化。
目的：探討芪薊腎康方通過JNK信號通路對大鼠腎小毬繫膜細胞的影響。方法：體外培養大鼠腎小毬繫膜細胞，用血管緊張素Ⅱ刺激繫膜細胞增生，給予芪薊腎康方黃酮榦預，用酶聯免疫吸附（ELISA）法檢測腎小毬繫膜細胞上清液 c-Jun 氨基末耑激酶（JNK）、活化蛋白1（AP-1）、纖維粘連蛋白（FN）蛋白錶達；實時定量 PCR 法檢測 JNK、AP-1 mRNA 的錶達。結果：與正常組比較，模型組及治療組大鼠腎小毬繫膜細胞中 JNK、AP-1及 FN 蛋白錶達明顯升高（P約0.05或 P約0.01）；與模型組比較，治療組大鼠腎小毬繫膜細胞中 JNK、AP-1及 FN 蛋白錶達明顯降低（P約0.05或 P約0.01）。與正常組比較，模型組及治療組大鼠腎小毬繫膜細胞中 JNK、AP-1及 FN mRNA 錶達明顯升高（P約0.05或 P約0.01）；與模型組比較，治療組大鼠腎小毬繫膜細胞中 JNK、AP-1及 FN mRNA明顯降低（P約0.05）。結論：芪薊腎康方可以通過下調腎小毬繫膜細胞JNK、AP-1 mRNA及蛋白的錶達水平，抑製 JNK 信號轉導，降低 AP-1的活性，減少 FN 的增殖，從而減輕 GMC 增生，延緩腎小毬的損傷，防止腎小毬的硬化。
목적：탐토기계신강방통과JNK신호통로대대서신소구계막세포적영향。방법：체외배양대서신소구계막세포，용혈관긴장소Ⅱ자격계막세포증생，급여기계신강방황동간예，용매련면역흡부（ELISA）법검측신소구계막세포상청액 c-Jun 안기말단격매（JNK）、활화단백1（AP-1）、섬유점련단백（FN）단백표체；실시정량 PCR 법검측 JNK、AP-1 mRNA 적표체。결과：여정상조비교，모형조급치료조대서신소구계막세포중 JNK、AP-1급 FN 단백표체명현승고（P약0.05혹 P약0.01）；여모형조비교，치료조대서신소구계막세포중 JNK、AP-1급 FN 단백표체명현강저（P약0.05혹 P약0.01）。여정상조비교，모형조급치료조대서신소구계막세포중 JNK、AP-1급 FN mRNA 표체명현승고（P약0.05혹 P약0.01）；여모형조비교，치료조대서신소구계막세포중 JNK、AP-1급 FN mRNA명현강저（P약0.05）。결론：기계신강방가이통과하조신소구계막세포JNK、AP-1 mRNA급단백적표체수평，억제 JNK 신호전도，강저 AP-1적활성，감소 FN 적증식，종이감경 GMC 증생，연완신소구적손상，방지신소구적경화。
This study was aimed to investigate the effects of Qi-Ji Shen-Kang (QJSK) on glomerular mesangial cell (GMC) through the c-Jun N-terminal kinase (JNK) signal pathway. GMC was cultured in vitro and the proliferation was induced with Angiotensin II (AngII). Then, QJSK was used to inhibit the proliferation. ELISA was used in the detection of protein expressions of JNK, activator protein-1 (AP-1) and fibronectin (FN). Q-PCR was used in the de-tection of expression of JNK and AP-1mRNA. The results showed that compared with the normal group, protein ex-pressions of JNK, AP-1 and FN of GMC among rats in the model group and the treatment group were obviously in-creased (P< 0.05 or P< 0.01). Compared with the model group, protein expressions of JNK, AP-1 and FN of GMC among rats in the treatment group were obviously decreased (P < 0.05 or P < 0.01). Compared with the normal group, expressions of JNK, AP-1 and FN mRNA of GMC among rats in the model group and the treatment group were obviously increased (P< 0.01 or P< 0.05). Compared with the model group, expressions of JNK, AP-1 and FN mRNA of GMC among rats in the treatment group were obviously decreased (P< 0.05). It was concluded that QJSK can downregulate expressions of JNK and AP-1 mRNA, as well as the protein expressions of JNK, AP1 and FN, in order to inhibit JNK signal pathway, decrease activity of AP-1, reduce FN proliferation. It relieved proliferation of GMC, slowed down glomerulus damnification, and prevented glomerular sclerosis.
