CAJ | 학술논문

目的：探讨滋补脾阴方药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组、糖尿病组、脾阴虚组、脾阴虚糖尿病组(病证组)、脾阴虚糖尿病＋滋补脾阴方药组(治疗组)。采用高脂饮食喂养4周联合小剂量链脲佐菌素注射方法建立2型糖尿病模型。在此基础上采用饮食不节、劳倦过度及灌服伤阴药方法建立脾阴虚糖尿病模型。治疗组给予滋补脾阴方药灌胃，其余各组给予等体积生理盐水灌胃，连续15 d。取大脑皮质、海马及胃、肝组织，采用Western blot观察各组丙酮酸脱氢酶1α(PDHE1α)蛋白表达变化。结果糖尿病组和病证组大鼠皮质PDHE1α表达低于空白组(P＜0.05)，治疗组皮质和胃组织PDHE1α较病证组升高(P＜0.05)。各组大鼠海马及肝组织中 PDHE1α蛋白表达差异无统计学意义(P＞0.05)。结论滋补脾阴方药能够调节大脑皮质及胃组织中PDHE1α蛋白表达，改善脾阴虚糖尿病认知功能障碍。
목적：탐토자보비음방약개선비음허당뇨병인지공능장애적작용궤제。방법장대서수궤분위공백조、당뇨병조、비음허조、비음허당뇨병조(병증조)、비음허당뇨병＋자보비음방약조(치료조)。채용고지음식위양4주연합소제량련뇨좌균소주사방법건립2형당뇨병모형。재차기출상채용음식불절、노권과도급관복상음약방법건립비음허당뇨병모형。치료조급여자보비음방약관위，기여각조급여등체적생리염수관위，련속15 d。취대뇌피질、해마급위、간조직，채용Western blot관찰각조병동산탈경매1α(PDHE1α)단백표체변화。결과당뇨병조화병증조대서피질PDHE1α표체저우공백조(P＜0.05)，치료조피질화위조직PDHE1α교병증조승고(P＜0.05)。각조대서해마급간조직중 PDHE1α단백표체차이무통계학의의(P＞0.05)。결론자보비음방약능구조절대뇌피질급위조직중PDHE1α단백표체，개선비음허당뇨병인지공능장애。
Objective To explore the mechanism of Zibu Piyin Recipe (ZBPYR) on spleen yin deficiency diabetes-associated cognitive disorder (DACD). Methods The rats were randomly divided into control group, diabetes mellitus (DM) group, spleen yin deficiency group, spleen yin deficiency DM group and spleen yin deficiency DM+ZBPYR group (treatment group). Type 2 DM models were established by high-fat food feeding and low dose STZ intraperitoneal injection for 4 weeks. Then the classical compound method was used to construct spleen yin deficiency rat models by improper diet, over exertion and yin fluids exhaustion. The treatment group was given ZBPYR by gavage for 15 days, and the other groups were given the same amount of normal saline. Then cerebral cortex, hippocampus, stomach and liver were obtained and the changes of protein expression of PDHE1α in them were observed by Western Blot. Results The protein expression of PDHE1αin cortex of DM group and spleen yin deficiency DM group were lower than control group (P<0.05). PDHE1α expression of treatment group in cortex and stomach increased more significantly than spleen yin deficiency DM group (P<0.05). The expression of PDHE1α protein showed no significant difference among all groups in hippocampus and liver. Conclusion ZBPYR improved spleen yin deficiency DACD by regulating PDHE1αin cortex and stomach.