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黄芪甲苷通过 BDNF-TrkB 信号通路改善 MCAO 大鼠的神经行为,促进海马神经发生。

Astragaloside IV improves neurobehavior and promotes hippocampal neurogenesis in MCAO rats though BDNF-TrkB signaling pathway.

机构信息

Department of Rehabilitation, The Second Hospital of Hebei Medical University, No. 215, HePing Road, Shijiazhuang, 050000, Hebei Province, People's Republic of China.

Preclinical Medicine College of Hebei University of Chinese Medicine, No. 326, XinShiNan Road, Shijiazhuang, 050091, Hebei Province, People's Republic of China.

出版信息

Biomed Pharmacother. 2020 Oct;130:110353. doi: 10.1016/j.biopha.2020.110353. Epub 2020 Jul 16.

Abstract

Astragaloside IV (AST) as the main active ingredient of Astragalus membranaceus. Clinical and laboratory-based studies have demonstrated the effects of AST on cerebral protection and angiogenesis after ischemia stroke. In addition, several reports investigated the effect of AST on proliferation of neural stem cells. The current study was aimed to evaluate the influence of AST on neurogenesis in hippocampal dentate gyrus (DG) of MCAO rats and to explore the possible mechanisms. In this study, the neurobehavioral tests (Ludmila Belayev 12-point scoring, Screen test, fore limb placing test) had been employed to investigate the effect of AST treatment against functional deficit of MCAO rats. The immunofluorescence staining, western-blot and qRT-PCR was performed to evaluate the effects of AST on proliferation, differentiation and maturity of neural stemr cells in hippocampus. Moreover, we investigated the possible mechanism of the AST treatment in promoting neurogenesis after ischemic stroke. The findings indicated that AST treatment ameliorated the neurobehavior of MCAO rats. The results indicated that AST treatment possessed the potential to improve proprioceptive sense and motor function of MCAO rats. AST treatment sustained neuronal viability and stimulates sensorimotor integration functional recovery in MCAO rats. The results suggested that AST improved neurobehavior deficit after ischemic stroke. Furthermore, AST promoted neurogenesis through upregulating the expressing of BNDF/TrkB signaling pathway. Therefore AST might be a promising therapeutic agent for ischemic stroke.

摘要

黄芪甲苷(AST)是黄芪的主要活性成分。临床和实验室研究表明,AST 对缺血性脑卒中后的脑保护和血管生成有影响。此外,有几项报道研究了 AST 对神经干细胞增殖的影响。本研究旨在评估 AST 对 MCAO 大鼠海马齿状回(DG)神经发生的影响,并探讨可能的机制。在这项研究中,采用神经行为学测试(Ludmila Belayev 12 分评分、筛选测试、前肢放置测试)来研究 AST 治疗对 MCAO 大鼠功能缺陷的影响。免疫荧光染色、western blot 和 qRT-PCR 用于评估 AST 对海马神经干细胞增殖、分化和成熟的影响。此外,我们还研究了 AST 治疗在促进缺血性脑卒中后神经发生中的可能机制。研究结果表明,AST 治疗改善了 MCAO 大鼠的神经行为。结果表明,AST 治疗具有改善 MCAO 大鼠本体感觉和运动功能的潜力。AST 治疗维持 MCAO 大鼠神经元活力,并刺激感觉运动整合功能恢复。结果表明,AST 改善了缺血性脑卒中后的神经行为缺陷。此外,AST 通过上调 BDNF/TrkB 信号通路的表达促进神经发生。因此,AST 可能是缺血性脑卒中的一种有前途的治疗药物。

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