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Mechanism of Chuanxiong rhizoma regulating PI3K/AKT/FOXO1 signal axis in repairing vascular endothelial injury after ischemic stroke
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DOI   10.11656/j.issn.1673-9043.2026.09.07
Key Words   Chuanxiong Rhizoma;ischemic stroke;mice;angiogenesis;human brain microvascular endothelial cells
Author NameAffiliationE-mail
NING Ning Neurology Center, 942 Hospital of Joint Logistics Support force of Chinese People's Liberation Army, Yinchuan 750000, China  
DU Xiaojuan Department of Gastroenterology, 942 Hospital of Joint Logistics Support force of Chinese People's Liberation Army, Yinchuan 750000, China 19862686049@163.com 
LI Yunyun Neurology Center, 942 Hospital of Joint Logistics Support force of Chinese People's Liberation Army, Yinchuan 750000, China  
XUE Shengwen Neurology Center, 942 Hospital of Joint Logistics Support force of Chinese People's Liberation Army, Yinchuan 750000, China  
MA Jing Neurology Center, 942 Hospital of Joint Logistics Support force of Chinese People's Liberation Army, Yinchuan 750000, China  
Abstract
    [Objective] To explore the mechanism of Chuanxiong Rhizoma(CR) regulating phosphoinositide 3-kinase/protein kinase B/forkhead box O1(PI3K/AKT/FOXO1) signal axis in repairing vascular endothelial injury after ischemic stroke. [Methods] Human brain microvascular endothelial cells(HBMEC) were divided into the following four groups:blank(Con) group,oxygen-glucose deprivation/reoxygenation(OGD/R) group,CR group and CR+LY294002 group. Except Con group,other groups established OGD/R model. Except Con group,other groups established OGD/R model. Apoptosis was detected by flow cytometry,cell migration ability was detected by Transwell,and the ability of cells to form tubes was evaluated by tube formation test. 45 mice were randomly divided into Sham group,middle cerebral artery occlusion(MCAO) group and MCAO+CR group,with 15 mice in each group. Except Sham group,other groups established mouse MCAO models. The infarct area was analyzed by triphenyltetrazolium chloride(TTC) staining,the distribution of CD31 and PI3K in infarcted tissues was analyzed by immunofluorescence,and the signal expression of PI3K/AKT/FOXO1 was analyzed by protein blot. [Results] Compared with Con group,the number of apoptotic cells in HBMEC in OGD/R group increased significantly(P<0.05),and the number of cell migration and tube formation decreased significantly(P<0.05). Compared with OGD/R group,the number of apoptotic cells in HBMEC in CR group decreased significantly(P<0.05),while the number of cell migration,the number of tube formation and the expression of p-PI3K/PI3K,p-AKT/AKT,p-FOXO1/FOXO1 increased significantly(P<0.05). The number of apoptotic cells in HBMEC in CR+LY294002 group was higher than that in CR group(P<0.05),and the number of cell migration and tube formation was lower than that in CR group(P<0.05). Compared with Sham group,cerebral infarction area and neurological deficit score in MCAO group increased significantly(P<0.05). Compared with MCAO group,the cerebral infarction area and neurological deficit score in MCAO+CR group decreased significantly(P<0.05). The ratio of CD31+PI3K+ cells and the expressions of p-PI3K/PI3K,p-AKT/AKT and p-FOXO1/FOXO1 in MCAO+CR group were higher than those in MCAO group(P<0.05). [Conclusion] CR aqueous extract inhibits apoptosis and stimulates angiogenesis in OGD/R-stimulated HBMECs and MCAO-induced mice through modulating PI3K-AKT-FOXO1 signalling.

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