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Exploration of the mechanism of Compound Angelica Injection on mimicischemic neurons from PI3K/Akt and MAPK/Erk signal pathways
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DOI   10.11656/j.issn.1672-1519.2020.04.20
Key Words   mimic ischemia injury;neuron;Compound Argelica Injection;PI3K/Akt;MAPK/Erk;BMECs;ischemic stroke
Author NameAffiliationE-mail
LI Yunxin College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
TANG Yibo College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
ZHENG Yanfei College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
LI Yue School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China  
YU Xue College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
ZHANG Qiaohui College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
CHEN Yafei College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China  
BAI Xue School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China  
MA Ru School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China  
LIU Zhenquan School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China lzqbzy@sina.com 
Abstract
    [Objective] To investigate the effect and mechanism of Compound Angelica Injection(CAI) on conditioned medium after mimic ischemic brain microvascular endothelial cells(BMECs) on mimic ischemic injured neurons.[Methods] Primitive culture SD rats'BMECs and cortex neuron were identifiedby immunofluorescence. Normal BMECs conditioned medium (N-CM),mimic ischemic injury BMECs conditioned medium (I-CM) andmimic ischemic injury BMECs with different doses of CAI intervention conditioned medium (IC-CM,L=1.25 μL/mL,M=2.5 μL/mL,H=5 μL/mL) were collected,which applied to normal neurons and mimic ischemic neurons respectively. The activity of neurons in each group was detected by CCK-8 method and the phosphorylation level of Akt in PI3K/Akt signaling pathway (p-Akt/Akt)and Erk in MAPK/Erk signaling pathway (p-Erk/Erk) were detected by western blotting.[Results] Compared with N-CM treatment group,the neuronal activity of I-CM treatment group was significantly decreased (P<0.01). Akt phosphorylation level was decreased (P<0.05),Erk phosphorylation level increased significantly (P<0.01). After CAI intervention,the neuronal activity and Akt phosphorylation level in IC-CML group were higher than that in I-CM group (P<0.05). The activity of neurons and the phosphorylation level of Akt in the IC-CML and IC-CMH groups were significantly higher than those in the I-CM group (P<0.01). The phosphorylation level of Erk in each IC-CM group was not significantly different from that in the I-CM group(P>0.05).[Conclusion] CAI can protect the neurons of mimic ischemic injury by interfering with the endothelial cells of ischemic injury. The protective effect may be correlated with the activation of PI3K/Akt signaling pathway,but has little correlation with MAPK/Erk signaling pathway.

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