NEUROLOGY / RESEARCH PAPER
Effects of Zhuyu Annao on Hippocampal Neuronal Apoptosis and Cognitive Disorder in a Rat Model of Ischemic Brain Injury
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Lin Wu 1
 
 
 
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1
The First Affiliated Hospital of Guangxi University of Chinese Medicine, China
2
Graduate College of Guangxi University of traditional Chinese Medicine, China
CORRESPONDING AUTHOR
Lin Wu   

The First Affiliated Hospital of Guangxi University of Chinese Medicine, China
Submission date: 2020-04-21
Final revision date: 2020-12-23
Acceptance date: 2021-01-07
Online publication date: 2021-03-21
 
 
KEYWORDS
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ABSTRACT
Introduction:
We aimed to determine the effects of Zhuyu Annao (ZYAN) prescription on hippocampal neuronal apoptosis and cognitive disorder (CD) in ischemic brain injury (IBI).

Material and methods:
The improved Rice-Vannucci method was used to prepare a rat model of IBI. Rats in the ZYAN prescription group were intragastrically administered 12.50 g/kg of ZYAN prescription 4 h after modeling; rats in the mock surgical group (MSG) and model group (MG) were administered an intraperitoneal injection of the same volume of normal saline twice daily.

Results:
Compared with MG, the area of cerebral infarction, pathological changes, neuron apoptosis index, and neurodeficit score were significantly reduced in the ZYAN prescription group (P < 0.05). Morris water maze test showed that in the ZYAN prescription group, incubation period was significantly shortened and the number of platform crossings was significantly increased (P < 0.05). Furthermore, the rats in the ZYAN prescription group showed significantly reduced protein and mRNA expressions of cleaved caspase-3, Bax, p-53, and p38 mitogen-activated protein kinase (MAPK) in the hippocampus, whereas the protein and mRNA expressions of Bcl-2 were significantly increased (P < 0.05).

Conclusions:
ZYAN prescription reduced the area of cerebral infarction, attenuated neuronal apoptosis, and alleviated CD in the rats with IBI. The beneficial effect of ZYAN prescription in IBI may be mediated via the inhibition of the p38 MAPK signaling pathway and caspase-3 cascade reaction.

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ISSN:1734-1922