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Study on the effect of Erigeron Breviscapus Injection on neural injury in stroke rats by regulating the JAK2/STAT3 signaling pathway
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DOI   10.11656/j.issn.1672-1519.2024.02.13
Key Words   Erigeron Breviscapus Injection;stroke;janus kinase 2/signal transducer and activator of transcription 3;neuroprotection
Author NameAffiliationE-mail
ZHAO Qian Department of Neurology, Zhengzhou Seventh People's Hospital, Zhengzhou 450016, China  
ZENG Limin Department of Neurology, Zhengzhou Seventh People's Hospital, Zhengzhou 450016, China  
ZHOU Liping Department of Neurology, Zhengzhou Seventh People's Hospital, Zhengzhou 450016, China  
QI Lin Department of Laboratory, Zhengzhou Seventh People's Hospital, Zhengzhou 450016, China 614242286@qq.com 
Abstract
    [Objective] To investigate the neuroprotective effect of Erigeron Breviscapus Injection(EBI) on stroke rats and its regulatory mechanism on the JAK2/STAT3 signaling pathway during this process. [Methods] A rat model of ischemic stroke was established using middle cerebral artery occlusion(MCAO),and the successfully modeled rats were randomly grouped into model group,nimodipine group,EBI group,JAK2 inhibitor group(AG490 group),and EBI+JAK2 agonist group(EBI+CA1 group),with 20 rats in each group. In addition,20 rats were selected as sham surgery group,which only exposed carotid artery without ligation. The neurological deficit score was applied to evaluate the neural function of rats;TTC staining was applied to detect the area of cerebral infarction in rats;HE and Nissl staining were applied to detect the pathological morphology of rat brain tissue;TUNEL staining was applied to detect neuronal apoptosis in rat brain tissue;ELISA was applied to detect the levels of SOD,GSH-Px,and MDA in rat brain tissue;and Western blot was applied to detect the expression of Bax,Bcl-2,and JAK2,p-JAK2,STAT3,and p-STAT3 proteins in rat brain tissue. [Results] Compared with the sham surgery group,the cerebral infarction size of rats in the model group increased,neuronal apoptosis rate increased,nerve defect score,MDA level,Bax protein expression,p-JAK2/JAK2,p-STAT3/STAT3 ratio increased(P<0.05),meanwhile,neurons in brain tissue degenerated and the number of neurons decreased,the activities of SOD and GSH-Px and the expression of Bcl-2 protein were decreased(P<0.05);compared with the model group,the area of cerebral infarction,apoptosis rate of neurons increased,nerve defect score,MDA level,Bax protein,p-JAK2/JAK2 and p-STAT3/STAT3 ratio in the EBI group,nimodipine group,and AG490 group decreased(P<0.05),meantime,neuronal damage in brain tissue was reduced,and the number of neurons,SOD and GSH-Px activities,Bcl-2 protein expression increased(P<0.05);further use of JAK2 agonists for compensatory experiments revealed that the protective effect of EBI on nerve injury in rats was reversed(P<0.05). [Conclusion] EBI can reduce nerve damage in stroke rats by inhibiting the JAK2/STAT3 signaling pathway.

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