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| Effect of Apigenin on angiogenesis and neurogenesis in the cerebral ischemic penumbra of middle cerebral artery occlusion rat via VEGF signaling pathway |
| LIU Chan, HU Quan, XIE Qingfeng, ZHU Anqi, CHEN Xiang. |
| Department of Children Rehabilitation, the Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325000, China |
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| Cite this article: |
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LIU Chan,HU Quan,XIE Qingfeng, et al. Effect of Apigenin on angiogenesis and neurogenesis in the cerebral ischemic penumbra of middle cerebral artery occlusion rat via VEGF signaling pathway[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2023, 53(3): 182-188.
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Abstract Objective: To investigate the effects of Apigenin (APG)-induced angiogenesis and neurogenesis in the cerebral ischemic penumbra of middle cerebral artery occlusion (MCAO) rats and whether these changes involve the vascular endothelial growth factor (VEGF) signaling pathway. Methods: A total of 144 adult male Sprague Dawley rats were randomly divided into sham operation group (groups S7 and S14, respectively), a model group (groups M7 and M14, respectively), an APG treatment model group (groups AM7 and AM14,respectively), and an APG+VEGF-R inhibitor treatment model group (groups AIM7 and AIM14, respectively).A MCAO animal model was established; neurobehavioral performance and infarct volumes were assessed using the modified neurological severity score (mNSS) and 2, 3, 5‑triphenyl tetrazolium chloride staining; VEGF expression levels, and changes in angiogenesis and new neurons in the cerebral ischemic penumbra were evaluated using Western blot analysis, immunohistochemistry, and immunofluorescence. Results: Compared with the S group, the neurologic impairment symptoms and white infarcts were observed in the M group, AM group and AIM group; the neurological scores and infarct volume in the AM group were significantly decreased compared with those in the M group at the same time-point (P<0.05). The VEGF expression in the AM group was increased compared with that in the M group at the same time-point (P<0.01), and microvessel density was increased in the AM7 group compared with that in the M7 group (P<0.05). The number of bromodeoxyuridine (BrdU)/nestin and BrdU/NeuN double-labeled positive cells in the AM group were significantly increased compared with those in the M group at the same time-point (P<0.01). VEGF-R inhibitors reversed the improvement effect of APG. Conclusion: APG ameliorates focal cerebral ischemia/reperfusion-induced neurological deficit by promoting angiogenesis and neurogenesis through upregulation of the VEGF signaling pathway.
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Received: 10 December 2022
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