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
2015年
6期
1189-1193
,共5页
梁丽娜%战丽彬%胡守玉%隋华%陈静
樑麗娜%戰麗彬%鬍守玉%隋華%陳靜
량려나%전려빈%호수옥%수화%진정
自噬%内质网应激%脾阴虚糖尿病认知功能障碍%滋补脾阴方药%下丘脑
自噬%內質網應激%脾陰虛糖尿病認知功能障礙%滋補脾陰方藥%下丘腦
자서%내질망응격%비음허당뇨병인지공능장애%자보비음방약%하구뇌
Autophagy%endoplasmic reticulum stress%spleen-yin deficiency diabetes-associated cognitive decline%Zi-Bu Pi-Yin recipe%hypothalamus
目的:探讨滋补脾阴方药(ZBPYR)调节自噬及内质网应激(ERS)改善脾阴虚糖尿病认知功能障碍的作用机制。方法:将大鼠随机分为空白对照组(cont),糖尿病组(DM),脾阴虚组(pi),脾阴虚糖尿病组(piDM),脾阴虚糖尿病+滋补脾阴方药治疗组(ZBPYR)。Western Blot观察微管相关蛋白1A/1B轻链3Ⅱ(LC3Ⅱ)、抑制物阻抗性酯酶1α亚基(IRE1α)、c-Jun氨基端激酶(JNK)的蛋白表达。结果:DM组、pi组、piDM组LC3Ⅱ较cont组降低(P<0.05),ZBPYR组LC3Ⅱ较DM组、piDM组增加(P<0.05)。与cont组比较,DM组、piDM组p-IRE1α、pi组、piDM组p-JNK1均有所增加(P<0.05),ZBPYR组p-IRE1α、p-JNK1与DM组、piDM组比较有所降低(P<0.05)。结论:ZBPYR调节自噬及ERS改善脾阴虚糖尿病认知功能障碍。
目的:探討滋補脾陰方藥(ZBPYR)調節自噬及內質網應激(ERS)改善脾陰虛糖尿病認知功能障礙的作用機製。方法:將大鼠隨機分為空白對照組(cont),糖尿病組(DM),脾陰虛組(pi),脾陰虛糖尿病組(piDM),脾陰虛糖尿病+滋補脾陰方藥治療組(ZBPYR)。Western Blot觀察微管相關蛋白1A/1B輕鏈3Ⅱ(LC3Ⅱ)、抑製物阻抗性酯酶1α亞基(IRE1α)、c-Jun氨基耑激酶(JNK)的蛋白錶達。結果:DM組、pi組、piDM組LC3Ⅱ較cont組降低(P<0.05),ZBPYR組LC3Ⅱ較DM組、piDM組增加(P<0.05)。與cont組比較,DM組、piDM組p-IRE1α、pi組、piDM組p-JNK1均有所增加(P<0.05),ZBPYR組p-IRE1α、p-JNK1與DM組、piDM組比較有所降低(P<0.05)。結論:ZBPYR調節自噬及ERS改善脾陰虛糖尿病認知功能障礙。
목적:탐토자보비음방약(ZBPYR)조절자서급내질망응격(ERS)개선비음허당뇨병인지공능장애적작용궤제。방법:장대서수궤분위공백대조조(cont),당뇨병조(DM),비음허조(pi),비음허당뇨병조(piDM),비음허당뇨병+자보비음방약치료조(ZBPYR)。Western Blot관찰미관상관단백1A/1B경련3Ⅱ(LC3Ⅱ)、억제물조항성지매1α아기(IRE1α)、c-Jun안기단격매(JNK)적단백표체。결과:DM조、pi조、piDM조LC3Ⅱ교cont조강저(P<0.05),ZBPYR조LC3Ⅱ교DM조、piDM조증가(P<0.05)。여cont조비교,DM조、piDM조p-IRE1α、pi조、piDM조p-JNK1균유소증가(P<0.05),ZBPYR조p-IRE1α、p-JNK1여DM조、piDM조비교유소강저(P<0.05)。결론:ZBPYR조절자서급ERS개선비음허당뇨병인지공능장애。
This study was aimed to explore the mechanism ofZi-Bu Pi-Yin Recipe (ZBPYR) on autophagy and endoplasmic reticulum stress (ERS) to improve spleen-yin deficiency diabetes-associated cognitive decline (DACD). Rats were randomly divided into the control (cont) group, the diabetes (DM) group, the spleen-yin deficiency (pi) group, the spleen-yin deficiency diabetes (piDM) group, and the spleen-yin deficiency diabetes + ZBPYR treatment (ZBPYR) group. The expression of microtubule-associated protein 1A/1B-light chain 3 (LC3Ⅱ), inositol-requiring enzymeα (IRE1α), c-Jun N-terminal kinase (JNK) were observed by western blot. The results showed that the expression of LC3Ⅱ in the DM group, pi group and piDM group decreased compared with the cont group (P < 0.05); and the expression of LC3Ⅱ of the ZBPYR group increased compared with the DM group and piDM group (P < 0.05). Compared with the cont group, the p-IRE1α of the DM group and piDM group, as well as p-JNK1 in the pi group and piDM group were increased (P < 0.05). The p-IRE1α and p-JNK1 of the ZBPYR group were decreased compared with the DM group and piDM group (P < 0.05). It was concluded that ZBPYR improved spleen-yin deficiency DACD by regulating autophagy and ERS.