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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 investigate the effect of proanthocyanidins on Aβ, tau and superoxide dismutase (SOD) in the hippocampus of Alzheimer’s disease-induced rats induced by D-gal and aluminum trichloride (AlCl3). Methods: Alzheimer’s disease model was established by D-gal intraperitoneal injection (i.p.) 180mg · kg-1 · d-1 and AlCl3 intragastric administration (15mg · kg-1 · d-1) The successful model rats were randomly divided into model group, vitamin E group, proanthocyanidin low-dose group, proanthocyanidin high-dose group, another set of blank control group. After modeling, the rats were gavaged once a day for 8 weeks. After the last administration, the rats were sacrificed and the hippocampus of rats were sacrificed. The expression of Aβ, SOD and tau protein was detected by Western blot. Results: Compared with the blank control group, the expression of Aβ and tau in model group increased significantly and the expression of SOD protein decreased significantly (P <0.01). Compared with the model group, the expression of Aβ and tau decreased and SOD protein increased with the increase of proanthocyanidin dose (P <0.01, P <0.05). CONCLUSION: Proanthocyanidins can improve hippocampal lesion in AD rats induced by D-gal and AlCl3, and its mechanism may be related to the increase of SOD activity in hippocampus.