CAJ | 학술논문

目的：观察脾阴虚糖尿病大鼠海马及大脑皮质中不同形式的β淀粉样蛋白（Aβ）、胰岛素降解酶（IDE）变化，及其在脾阴虚糖尿病认知功能障碍中的作用，并观察滋补脾阴法对其影响。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）、滋补脾阴方药治疗组（ZBPYR）5组。采用梯度离心的方法提取可溶性与不可溶Aβ，通过ELISA方法测定各组大鼠海马及大脑皮质中可溶性与不可溶的Aβ1-42及Aβ1-40的含量变化，通过Western blot方法观察各组大鼠海马及皮质中IDE蛋白表达变化。结果：DM组、piDM组大鼠海马、大脑皮质可溶性与不可溶Aβ1-42均高于Cont组（P<0.05），ZBPYR组较DM组、piDM组降低了海马、大脑皮质可溶性与不可溶Aβ1-42的表达（P<0.05）。DM组、pi组、piDM组大脑皮质可溶性Aβ1-40较Cont组增加（P<0.05），ZBPYR组较DM组、piDM组有所下降（P<0.05）。DM组、piDM组海马IDE蛋白表达较Cont组降低（P<0.05），ZBPYR组海马较DM组、piDM组升高（P<0.05）；DM组、pi组、piDM组大鼠大脑皮质IDE蛋白水平较Cont组降低（P<0.05），ZBPYR组大脑皮质较DM组降低（P<0.05）。结论：脑组织中Aβ1-42增加可能是糖尿病大鼠、脾阴虚糖尿病大鼠认知功能障碍的主要病理变化，IDE表达下降可能是导致Aβ1-42增加的原因之一，滋补脾阴法可能通过上调IDE蛋白表达降低Aβ1-42的含量。
목적：관찰비음허당뇨병대서해마급대뇌피질중불동형식적β정분양단백（Aβ）、이도소강해매（IDE）변화，급기재비음허당뇨병인지공능장애중적작용，병관찰자보비음법대기영향。방법：장대서수궤분위공백대조조（Cont）、당뇨병조（DM）、비음허조（pi）、비음허당뇨병조（piDM）、자보비음방약치료조（ZBPYR）5조。채용제도리심적방법제취가용성여불가용Aβ，통과ELISA방법측정각조대서해마급대뇌피질중가용성여불가용적Aβ1-42급Aβ1-40적함량변화，통과Western blot방법관찰각조대서해마급피질중IDE단백표체변화。결과：DM조、piDM조대서해마、대뇌피질가용성여불가용Aβ1-42균고우Cont조（P<0.05），ZBPYR조교DM조、piDM조강저료해마、대뇌피질가용성여불가용Aβ1-42적표체（P<0.05）。DM조、pi조、piDM조대뇌피질가용성Aβ1-40교Cont조증가（P<0.05），ZBPYR조교DM조、piDM조유소하강（P<0.05）。DM조、piDM조해마IDE단백표체교Cont조강저（P<0.05），ZBPYR조해마교DM조、piDM조승고（P<0.05）；DM조、pi조、piDM조대서대뇌피질IDE단백수평교Cont조강저（P<0.05），ZBPYR조대뇌피질교DM조강저（P<0.05）。결론：뇌조직중Aβ1-42증가가능시당뇨병대서、비음허당뇨병대서인지공능장애적주요병리변화，IDE표체하강가능시도치Aβ1-42증가적원인지일，자보비음법가능통과상조IDE단백표체강저Aβ1-42적함량。
This study was aimed to observe different forms of β-amyloid peptide (Aβ) and insulin degrading enzyme (IDE) in the hippocampus and cortex in order to further explore the role of Aβ and IDE on spleen yin deficiency di-abetes-associated cognitive decline (DACD), and the effect of Zi-Bu Pi-Y in method. The rats were randomly divided into five groups, which were the blank control (Cont) group, diabetes (DM) group, spleen yin deficiency (pi) group, spleen yin deficiency diabetes (piDM) group and Zi-Bu Pi-Y in recipe (ZBPYR) group. Soluble and insoluble Aβ in the hippocampus and cortex of rats were extracted by gradient centrifugation, and then measured by ELISA. The ex-pression of IDE was observed by western blot. The results showed that the content of soluble and insoluble Aβ1-42 in the hippocampus and cortex of the DM group and piDM group were higher than the Cont group. The soluble and in-soluble Aβ1-42 content in the hippocampus and cortex of the ZBPYR group were reduced compared with the DM group and the piDM group. The soluble Aβ1-40 in the cortex of the DM group, pi group and piDM group were in-creased compared with the Cont group (P < 0.05). The soluble Aβ1-40 content of the ZBPYR group was decreased compared with the DM group and the piDM group (P < 0.05). The expression of IDE protein was decreased in the hippocampus of the DM group and the piDM group compared with the Cont group (P< 0.05), and the IDE protein level in the hippocampus of the ZBPYR group was increased compared with the DM group and the piDM group (P<0.05). The expression of IDE protein in the cortex of the DM group, pi group and piDM group was lower than the Cont group (P< 0.05). The IDE protein level in the cortex of the ZBPYR group was reduced compared to the DM group (P< 0.05). It was concluded that the increased Aβ1-42 in brain may be a major pathological change of DACD and spleen yin deficiency DACD. The decreased IDE expression may be one of the reasons to induce increasing of Aβ1-42 level. The Zi-Bu Pi-Y in method may decrease the Aβ1-42 content by upregulating IDE protein expression.