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首页> 外文期刊>Cellular Physiology and Biochemistry >Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia
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Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia

机译：丹酚酸B通过IGF-1 / Akt途径改善血管性痴呆大鼠的认知功能障碍。

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>BackgroundAims: Salvianolic acid B (SalB) is a natural polyphenolic compound enriched in Salvia miltiorrhiza Bunge. Our study was designed to explore the role of Sal B on cognitive impairment in vascular dementia (VD) model rats, as well as its possible molecular mechanisms. Methods: Rats were randomly divided into four groups (n = 15 for each group): Control group, Sal B group (normal Sprague Dawley rats treated with Sal B), VD group and VD + Sal B group. The VD group rats were established by permanent bilateral common carotid artery occlusion (BCCAO). Animals in the Control and Sal B group received the same operation without bilateral common carotid arteries occlusion. The animals in Sal B group and VD + Sal B group received Sal B (20 mg/kg) orally once a day for consecutive 6 weeks. We investigated the effects of SalB on BCCAO-induced cognitive deficits rats models via the Morris water maze experiment. To explore the mechanisms of Sal B on cognitive function, we detected the expression of IGF-1, Akt and p-Akt, and the rate of cell apoptosis in CA1 region. Results: Our results observed that hippocampal IGF-1 was decreased in VD model rats, while SalB reversed the alteration of IGF-1 levels. The expression of hippocampal Akt showed no significant difference between control and VD group, however, p-Akt level was significantly decreased in VD group. After 6 weeks of SalB treatment, p-Akt level was significantly increased. A large number of apoptotic neurons were found in VD model rats, while SalB prevented apoptosis of hippocampal neurons in CA1 region in VD model rats. Conclusion: SalB significantly ameliorated cognitive deficits in BCCAO-induced VD model rats. The potential mechanism underlying the protective effects may be mediated through IGF-1/Akt pathway.
机译：> 背景目标： 丹酚酸B（SalB）是富含丹参丹参的天然多酚化合物。我们的研究旨在探讨Sal B在血管性痴呆（VD）模型大鼠认知功能障碍中的作用及其可能的分子机制。 方法： 将大鼠随机分为四组（每组15只）：对照组，Sal B组（用Sal B治疗的正常Sprague Dawley大鼠），VD组和VD + Sal B组。通过永久性双侧颈总动脉闭塞（BCCAO）建立VD组大鼠。对照组和Sal B组的动物接受相同的手术，但没有双侧颈总动脉闭塞。 Sal B组和VD + Sal B组的动物连续6周每天口服一次Sal B（20 mg / kg）。我们通过莫里斯水迷宫实验研究了SalB对BCCAO诱导的认知缺陷大鼠模型的影响。为了探索Sal B认知功能的机制，我们检测了IGF-1，Akt和p-Akt的表达以及CA1区细胞凋亡的速率。 结果： 我们的结果发现，VD模型大鼠海马IGF-1降低，而SalB逆转了IGF-1水平的改变。对照组和VD组海马Akt的表达无明显差异，而VD组p-Akt水平明显降低。 SalB治疗6周后，p-Akt水平明显升高。在VD模型大鼠中发现了大量的凋亡神经元，而SalB阻止了VD模型大鼠CA1区海马神经元的凋亡。 结论： SalB明显改善了BCCAO诱发的VD模型大鼠的认知缺陷。保护作用的潜在机制可能是通过IGF-1 / Akt途径介导的。

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