CAJ | 학술논문

目的：观察黄连解毒汤有效部位（总生物碱、总黄酮、总环烯醚萜）对中动脉栓塞大鼠海马神经元的保护作用。并通过检测缺血中心区（尾壳核）和远隔脑区（海马）血管内皮生长因子VEGF的表达，探讨其作用机制。方法：建立中动脉栓塞大鼠模型，免疫荧光染色技术观察神经元核蛋白NeuN及血管内皮生长因子VEGF的表达。结果：脑缺血7 d大鼠海马神经元核蛋白NeuN表达下调，尾壳核、海马VEGF免疫染色强度降低，差异较假手术组有统计学意义（ P＜0．05）。黄连解毒汤水提取物和总黄酮可提高海马神经元NeuN表达（P＜0．05）；总生物碱、总黄酮、总环烯醚萜组大鼠海马CA1区VEGF表达较模型组增强（P＜0．05）；总黄酮还可明显上调尾壳核VEGF表达（ P＜0．01）。结论：黄连解毒汤总黄酮对缺血中心区、远隔脑区VEGF均有调节作用，可减轻脑梗死远隔部位海马CA1区神经元继发性损害。
목적：관찰황련해독탕유효부위（총생물감、총황동、총배희미첩）대중동맥전새대서해마신경원적보호작용。병통과검측결혈중심구（미각핵）화원격뇌구（해마）혈관내피생장인자VEGF적표체，탐토기작용궤제。방법：건립중동맥전새대서모형，면역형광염색기술관찰신경원핵단백NeuN급혈관내피생장인자VEGF적표체。결과：뇌결혈7 d대서해마신경원핵단백NeuN표체하조，미각핵、해마VEGF면역염색강도강저，차이교가수술조유통계학의의（ P＜0．05）。황련해독탕수제취물화총황동가제고해마신경원NeuN표체（P＜0．05）；총생물감、총황동、총배희미첩조대서해마CA1구VEGF표체교모형조증강（P＜0．05）；총황동환가명현상조미각핵VEGF표체（ P＜0．01）。결론：황련해독탕총황동대결혈중심구、원격뇌구VEGF균유조절작용，가감경뇌경사원격부위해마CA1구신경원계발성손해。
Objective:To investigate the effects of Huanglian Jiedu Decoction( HLJDDAF) which consists of total alkaloids, total fla-vonoids and total iridoids on the expression of VEGF in caudate putamen and hippocampal CA1 region of rats after middle cerebral artery occlusion and to explore the mechanism of the effects.Methods: Cerebral ischemia was induced by middle cerebral artery occlusion ( MACO) .The expressions of NeuN and VEGF were observed by immunofluorescence staining.Results:The expression of NeuN in dis-tant brain regions of rats in model group were significantly reduced, and the expression of VEGF in caudate putamen and hippocampal re-gion were reduced compared with those of the sham group( P<0.01-0.05) .Aqueous extract, total flavonoids were capable of increas-ing the expression of the NeuN compared with those of the model group(P<0.01-0.05);total alkaloids, total flavonoids and total iri-doids were capable of increasing the expression of the VEGF in hippocampal CA1 region compared with those of the model group( P<0.01-0.05).Especially the total flavonoids also increased the expression of VEGF in caudate putamen(P<0.01).Conclusion:Total flavonoids of HLJDD is inherently capable of regulating the expression of VEGF in caudate putamen and distant brain regions, and reduc-ing hematogenously secondary damage of hippocampal CA1 region after cerebral infarction.