摘要
目的:研究原花青素对D-半乳糖(D-gal)联合三氯化铝(AlCl3)诱导的阿尔茨海默病大鼠海马Aβ、tau和超氧化物歧化酶(SOD)的影响。方法:D-gal腹腔注射(i.p.)180mg·kg-1·d-1联合AlCl3灌胃(i.g.)15mg·kg-1·d-1 12周建立阿尔茨海默病模型。将造模成功大鼠随机分为模型组、维生素E组、原花青素低剂量组、原花青素高剂量组,另设空白对照组。造模后每日灌胃给相应药物一次,连续8周。于末次给药后处死,取大鼠海马部位脑组织,采用Western blot检测Aβ、SOD、tau蛋白表达。结果:与空白对照组相比,模型组Aβ、tau蛋白表达显著增加,SOD蛋白表达显著减少,差异有统计学意义(P<0.01)。与模型组相比,随着原花青素剂量的增加,大鼠Aβ、tau蛋白表达减少,SOD蛋白表达增加,差异有统计学意义(P<0.01,P<0.05)。结论:原花青素可改善D-gal联合AlCl3诱导的AD大鼠海马病变,其机制可能与提高海马SOD活性有关。
AIM： To observe the effects of proanthocyanidins on Aβ, tau and SOD with Alzheimer disease in rats. METHODS： AD model was mimicked by intraperitoneal injecting Dgal （180 mg· kg^-1 · d^-1） and intragastric administrating AlCl3 （15 mg · kg^-1 · d^-1 ） for 12 weeks. Then AD rats who were built successfully were randomly divided into 4 groups, model group, proanthocyanidins low-dose group, proanthocyanidins high-dose group, VitE group, but control group was set up by intraperitoneal injecting NS and intragastric administrating NS for 12 weeks, in additional. After that, each group was intragastric administrated with differ-ent drugs, control group （NS i.p. ）, model group（D-gal i.p. q.＋AlCl3 i. g. ）, proanthocyani-dins low-dose group （PC 20 mg/kg）, proanthocyanidins high-dose group （PC 40 mg/kg）, VitE group （VitE 10 mg/kg） for 8 weeks. The expression of Aβ, SOD, tau protein were detected with Western blot. RESULTS：As compared with control group, the expressions of Aβ and tau protein were higher and SOD was lower in model group （P〈0.01）. However, the expression of Aβ and tau protein decreased and SOD increased in proanthocyanidins high-close group （ 40 mg/kg）, there was statistically significant difference between PC high-dose group and model group （P〈0. 01, P〈0. 05）. CONCLUSION： Proanthocyanidins has protective effects on Alzheimer disease in rats.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2014年第3期280-283,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
安徽省高等学校省级优秀青年人才基金项目(2012SQRL124)
皖南医学院中青年基金资助项目(WK201019)
