CAJ | 학술논문

目的探讨血管内皮生长因子(VEGF)、P38MAPK在阿尔茨海默病(AD)模型大鼠中的发病机制及丁苯酞对AD模型大鼠海马组织VEGF、P38MAPK表达的影响.方法 32只SD大鼠按随机数字表法分为空白组、模型组、丁苯酞低剂量组和高剂量组,每组8只.采用凝聚态Aβ1-42双侧注射大鼠海马区制作AD模型,通过Morris水迷宫检测行为学改变,应用Western Blot技术测定大鼠海马VEGF、P38MAPK蛋白的表达.结果造模1周后,4组大鼠逃避潜伏期不同(F=66.658,P＜0.05),穿越平台次数不同(F =6.884,P＜0.05),模型组和药物干预组较空白组逃避潜伏期明显增长(P＜0.05),穿越平台次数明显减少(P＜0.05)；药物干预4周后,VEGF在4组大鼠海马区表达差异有统计学意义(F=171.064,P＜0.05),模型组较空白组明显降低(P＜0.05),药物干预组较模型组明显增多(P＜0.05),且高剂量组较低剂量组增多(P＜0.05)；P38MAPK在4组大鼠海马区表达差异无统计学意义(P＞0.05),P-P38MAPK在4组大鼠海马区表达差异有统计学意义(F=104.395,P ＜0.05),模型组和药物干预组较空白组海马组织P-P38MAPK表达升高(P＜0.05),药物干预组较模型组表达明显降低(P＜0.05),且高剂量组较低剂量组降低更明显(P＜0.05).结论丁苯酞能明显提高AD模型大鼠VEGF的表达,降低P-P38MAPK在AD大鼠海马组织的表达.
목적 탐토혈관내피생장인자(VEGF)、P38MAPK재아이자해묵병(AD)모형대서중적발병궤제급정분태대AD모형대서해마조직VEGF、P38MAPK표체적영향.방법 32지SD대서안수궤수자표법분위공백조、모형조、정분태저제량조화고제량조,매조8지.채용응취태Aβ1-42쌍측주사대서해마구제작AD모형,통과Morris수미궁검측행위학개변,응용Western Blot기술측정대서해마VEGF、P38MAPK단백적표체.결과 조모1주후,4조대서도피잠복기불동(F=66.658,P＜0.05),천월평태차수불동(F =6.884,P＜0.05),모형조화약물간예조교공백조도피잠복기명현증장(P＜0.05),천월평태차수명현감소(P＜0.05)；약물간예4주후,VEGF재4조대서해마구표체차이유통계학의의(F=171.064,P＜0.05),모형조교공백조명현강저(P＜0.05),약물간예조교모형조명현증다(P＜0.05),차고제량조교저제량조증다(P＜0.05)；P38MAPK재4조대서해마구표체차이무통계학의의(P＞0.05),P-P38MAPK재4조대서해마구표체차이유통계학의의(F=104.395,P ＜0.05),모형조화약물간예조교공백조해마조직P-P38MAPK표체승고(P＜0.05),약물간예조교모형조표체명현강저(P＜0.05),차고제량조교저제량조강저경명현(P＜0.05).결론 정분태능명현제고AD모형대서VEGF적표체,강저P-P38MAPK재AD대서해마조직적표체.
Objective To explore the roles of vascular endothelial growth factor (VEGF) and P38MAPK in the pathogenesis of Alzheimer's disease(AD) rats,and the effects of butyIphthalide on the influence of VEGF and P38MAPK in hippocampus of AD rats.Methods SD rats were randomly divided into blank group,AD model group,butylphthalide low-dose group and high dose group (n =8 rats per group).Aggregated Aβ1-42 was injected into the bilateral hippocampus of rats by stereotaxic coordinates method to induce AD.Morris water maze test was used to determine the abilities of learning and memory.Western blotting combined with Gel Doc imagine systems were used to investigate the expression of VEGF and P-P38MAPK in hippocampus of AD rats.Results The result of Morris water maze experiment showed that one week after modeling,escape latency was different(F =66.658,P ＜ 0.05),and either dose the frequency of crossing platform (F =6.884,P ＜0.05).Compared with the blank group,the other three groups'latent period of escape was extended significantly(P ＜ 0.05),and frequency of crossing platform was significantly less (P ＜ 0.05).After drug intervention for 4 weeks,the expression of VEGF was difference(F =171.064,P ＜0.05),it was decreased obviously in the model group than blank group(P ＜=0.05),but it was increased in the drug intervention groups than model group (P ＜ 0.05),and increased more significantly in the high dose group than low dose group (P ＜ 0.05).The expression of P38MAPK had no obvious change among four groups (P ＞ 0.05),however,the expression of P-P38MAPK showed difference(F =104.395,P ＜ 0.05),it was increased in drug intervention and model group than blank group (P ＜ 0.05),it was increased in drug intervention and model group than blank group (P ＜ 0.05),reduced significantly in drug intervention groups than model group (P ＜ 0.05),and decreased more significantly in high dose groups than low dose group (P ＜ 0.05).Conclusions Butylphthalide could obviously enhance the expression of VEGF,reduce the expression of P-P38MAPK in hippocampus of AD rats.