Luo Lin, Deng Shuhua, Yi Jian, Zhou Sainan, She Yan, Liu Baiyan
Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
Hunan University of Chinese Medicine, Changsha, Hunan 410208, China; Yiyang Medical College, Yiyang, Hunan 413000, China.
Evid Based Complement Alternat Med. 2017;2017:4072658. doi: 10.1155/2017/4072658. Epub 2017 Mar 8.
The aim of the present research is to investigate the therapeutic effect of Buyang Huanwu Decoction (BHD) in poststroke depression (PSD) animal model and illustrate its underlying mechanism via promoting neurotrophic pathway mediated neuroprotection and neurogenesis. To induce PSD rat model, isolation housed rats that received middle cerebral artery occlusion (MCAO) surgery successively suffered from chronic mild stress (CMS) treatment for consecutive twenty-one days. Meanwhile, rats were correspondingly given vehicle, BHD, and fluoxetine. Then, neurologic function was scored and depressive-like behaviors were assessed by sucrose preference test, locomotor activity, novelty-suppressed feeding test, and forced swim test. Thereafter, the neuroprotection and neurogenesis related molecular markers and signaling were detected. We firstly observed a significant neurological function recovery and antidepressants effect of BHD after MCAO together with CMS treatment. Our study also found that treatment with BHD and fluoxetine can significantly rescue neurons from apoptosis and promote neurogenesis in the CA3 and DG regions in the hippocampus. Notably, BHD and fluoxetine treatment can activate BDNF/ERK/CREB signaling. The results suggest that BHD is a promising candidate for treating PSD. Its curative effects can be attributed to neurotrophic pathway mediated neuroprotection and neurogenesis.
本研究旨在探讨补阳还五汤(BHD)对脑卒中后抑郁(PSD)动物模型的治疗作用,并通过促进神经营养途径介导的神经保护和神经发生来说明其潜在机制。为诱导PSD大鼠模型,将接受大脑中动脉闭塞(MCAO)手术的单独饲养的大鼠连续21天接受慢性轻度应激(CMS)处理。同时,相应地给予大鼠溶剂、BHD和氟西汀。然后,对神经功能进行评分,并通过蔗糖偏好试验、运动活动、新奇抑制摄食试验和强迫游泳试验评估抑郁样行为。此后,检测与神经保护和神经发生相关的分子标志物和信号传导。我们首先观察到在MCAO联合CMS处理后,BHD具有显著的神经功能恢复和抗抑郁作用。我们的研究还发现,BHD和氟西汀治疗可显著挽救神经元免于凋亡,并促进海马CA3和DG区的神经发生。值得注意的是,BHD和氟西汀治疗可激活BDNF/ERK/CREB信号传导。结果表明,BHD是治疗PSD的有前途的候选药物。其疗效可归因于神经营养途径介导的神经保护和神经发生。