Combination of Radix Astragali and Safflower Promotes Angiogenesis in Rats with Ischemic Stroke via Silencing PTGS2.
Combination of Radix Astragali and Safflower Promotes Angiogenesis in Rats with Ischemic Stroke via Silencing PTGS2.
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DOI：
10.3390/ijms24032126
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发表时间：
2023-01-21
影响因子：
5.6
通讯作者：
He, Yu
中科院分区：
文献类型：
--
作者：
Xu, Shouchao;Yang, Jiehong;Wan, Haitong;Yu, Li;He, Yu
促进缺血半暗带血管新生和恢复血流是治疗缺血性卒中（IS）的有效方法。黄芪-红花是活血化瘀的经典药对，在我国用于治疗IS已有数千年历史。即使如此，AS治疗IS的机制仍然是不可破译的。本研究首次从网络药理学的角度揭示了AS治疗IS的机制，表明AS可能通过抑制PTGS 2表达促进血管生成。以大脑中动脉闭塞/再灌注（MCAO/R）模型大鼠为实验动物，对预测结果进行验证。实验结果表明，AS可改善脑梗死体积、神经功能损害和脑组织病理学损害，抑制细胞凋亡，增加PDGF-BB、EPO和TGF-β1的含量，降低血清中PF 4、Ang-2和TIMP-1的水平。免疫组织化学染色显示PTGS 2在MCAO/R大鼠海马和大脑皮质的表达显著增加，而AS治疗可逆转这一趋势。免疫荧光染色显示AS逆转了VEGF的下调，并进一步促进了CD 31的表达，表明AS促进了MCAO/R大鼠血管生成。AS或塞来昔布（PTGS 2抑制剂）可逆转PTGS 2、PGI 2、bFGF、TSP-1和VEGF在半影区的异常蛋白或mRNA表达。结论：AS对IS的保护机制可能与抑制PTGS 2表达有关。
Promotion of angiogenesis and restoration of the blood flow in the ischemic penumbra is an effective treatment for patients with ischemic stroke (IS). Radix astragali-safflower (AS), a classic herbal pair for accelerating blood circulation and dispersing blood stasis, has been used for thousands of years to treat patients with IS in China. Even so, the mechanism of the treatment of IS by AS is still undecipherable. In the current study, network pharmacology was firstly employed to unveil the mechanism of AS in treating IS, which showed that AS might promote angiogenesis associated with PTGS2 silence. Middle cerebral artery occlusion/reperfusion (MCAO/R) model rats were then used as the experimental animals to verify the prediction result. The experimental results revealed that treatment with AS improved the cerebral infarct volume, neurological damage, and cerebral histopathological damage; inhibited cell apoptosis; increased the contents of PDGF-BB, EPO, and TGF-β1; and reduced the levels of PF4, Ang-2, and TIMP-1 in serum. Immunohistochemical staining demonstrated that the expression of PTGS2 was dramatically increased in the hippocampus and cerebral cortex of rats with MCAO/R, and this trend was reversed by the treatment of AS. Immunofluorescent staining expressed that AS reversed the down-regulation of VEGF and further promoted the expression of CD31, which indicated that AS promoted angiogenesis in MCAO/R rats. The abnormal protein or mRNA expression of PTGS2, PGI2, bFGF, TSP-1, and VEGF in the penumbra were transposed by AS or Celecoxib (an inhibitor of PTGS2). In conclusion, the protective mechanism of AS for IS promoted angiogenesis and was involved with PTGS2 silence.
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影响因子：
4.7
作者：
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通讯作者：
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影响因子：
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影响因子：
5.4
作者：
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