<br>梓醇通过 SDF-1α/CXCR4 途径促进神经发生和血管生成，从而减轻缺血性中风,Phytomedicine

当前位置： X-MOL 学术 › Phytomedicine › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

梓醇通过 SDF-1α/CXCR4 途径促进神经发生和血管生成，从而减轻缺血性中风
Phytomedicine ( IF 6.7 ) Pub Date : 2024-01-15 , DOI: 10.1016/j.phymed.2024.155362
Mei-Feng Zhang ₁ , Jing-Hui Wang ₁ , Si Sun ₁ , Yi-Tong Xu ₁ , Dong Wan ₂ , Shan Feng ₁ , Zhen Tian ₁ , Hui-Feng Zhu ₁

Affiliation

中风是全世界残疾和死亡的主要原因。目前，临床上缺乏针对缺血性中风后脑损伤的有效治疗方法。梓醇是一种源自中药的生物活性化合物，对多种神经系统疾病具有保护作用。然而，梓醇抗缺血性中风的潜在作用仍不完全清楚。本研究旨在进一步阐明梓醇对缺血性中风的保护作用。建立大鼠永久性大脑中动脉闭塞（pMCAO）和氧糖剥夺（OGD）模型来分别评估梓醇和氧糖剥夺的效果。采用行为测试来检查梓醇对缺血大鼠神经功能的影响。免疫染色评估各组神经干细胞（NSC）的增殖、迁移和分化以及血管生成。通过western blot检测相关分子的蛋白水平。还通过类似的方法检查了梓醇对培养的 NSC 以及 OGD 处理的脑微血管内皮细胞 (BMEC) 的影响。梓醇减轻了缺血大鼠的神经缺陷并改善了神经功能。它刺激室下区（SVZ）神经干细胞的增殖，促进其迁移至缺血皮质并分化为神经元或神经胶质细胞。同时，梓醇增加了缺血大鼠梗塞皮层的脑血管密度和增殖的脑血管内皮细胞的数量。研究发现，梓醇治疗可提高缺血皮质中 SDF-1α 和 CXCR4 的水平。梓醇还被证明可以促进培养的 NSC 的增殖和迁移，以及在 OGD 损伤下的 BMEC 的增殖。有趣的是，梓醇对培养细胞的影响被CXCR4抑制剂AMD3100抑制。此外，含有梓醇的BMECs培养基促进了NSCs的增殖，AMD3100也抑制了NSCs的增殖。我们的数据表明，梓醇通过 SDF-1α/CXCR4 途径促进神经发生和血管生成来发挥神经保护作用，这表明梓醇在治疗脑缺血方面具有治疗潜力。

"点击查看英文标题和摘要"

Catalpol attenuates ischemic stroke by promoting neurogenesis and angiogenesis via the SDF–1α/CXCR4 pathway

Stroke is a leading cause of disability and death worldwide. Currently, there is a lack of clinically effective treatments for the brain damage following ischemic stroke. Catalpol is a bioactive compound derived from the traditional Chinese medicine and shown to be protective in various neurological diseases. However, the potential roles of catalpol against ischemic stroke are still not completely clear. This study aimed to further elucidate the protective effects of catalpol against ischemic stroke. A rat permanent middle cerebral artery occlusion (pMCAO) and oxygen–glucose deprivation (OGD) model was established to assess the effect of catalpol and respectively. Behavioral tests were used to examine the effects of catalpol on neurological function of ischemic rats. Immunostaining was performed to evaluate the proliferation, migration and differentiation of neural stem cells (NSCs) as well as the angiogenesis in each group. The protein level of related molecules was detected by western–blot. The effects of catalpol on cultured NSCs as well as brain microvascular endothelial cells (BMECs) subjected to OGD were also examined by similar methods. Catalpol attenuated the neurological deficits and improved neurological function of ischemic rats. It stimulated the proliferation of NSCs in the subventricular zone (SVZ), promoted their migration to the ischemic cortex and differentiation into neurons or glial cells. At the same time, catalpol increased the cerebral vessels density and the number of proliferating cerebrovascular endothelial cells in the infracted cortex of ischemic rats. The level of SDF–1α and CXCR4 in the ischemic cortex was found to be enhanced by catalpol treatment. Catalpol was also shown to promote the proliferation and migration of cultured NSCs as well as the proliferation of BMECs subjected to OGD insult in . Interestingly, the impact of catalpol on cultured cells was inhibited by CXCR4 inhibitor AMD3100. Moreover, the culture medium of BMECs containing catalpol promoted the proliferation of NSCs, which was also suppressed by AMD3100. Our data demonstrate that catalpol exerts neuroprotective effects by promoting neurogenesis and angiogenesis via the SDF–1α/CXCR4 pathway, suggesting the therapeutic potential of catalpol in treating cerebral ischemia.

更新日期：2024-01-15

点击分享查看原文

点击收藏

阅读更多本刊新发论文本刊介绍/投稿指南