Publication: Electroacupuncture ameliorates learning and memory impairment by inhibiting inflammation and promoting synaptic plasticity via inhibition of the NF-KB/NLRP3 signaling pathway in cerebral ischemic rats
Authors
Guoyuan Pan ; Dan Lu1 ; Mingjin Zhu ; Guifen Yang ; Chenyi Huang ; Yisu Shou ; Xiong Jiangnan ; Fang Luo ; Sun Di ; Chuchu Huang
item.page.secondaryauthor
item.page.director
Publisher
publication.page.editor
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
publication.page.department
DOI
https://doi.org/10.14670/HH-18-997
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Objective. Electroacupuncture (EA) has a
protective effect on cerebral ischemic injury. However,
the specific mechanism of action of EA has not been
studied. In this study, we investigated whether EA was
involved in the treatment of learning and memory
impairment in rats with cerebral ischemia‒reperfusion
injury (CIRI) through the NF-KB/NLRP3 signaling
pathway.
Methods. Ninety-five male Sprague–Dawley (SD)
rats were randomly divided into five groups, each
consisting of 19 rats. A rat model of cerebral ischemia
was established using transient middle cerebral artery
occlusion (tMCAO) combined with cerebral blood flow
monitoring. Intervention treatments consisted of
electroacupuncture and lipopolysaccharide (an NF-κB
agonist) injection. The behavior, spatial learning, and
memory ability of the rats were evaluated with the
Morris water maze method. The degree of brain injury in
the rats was observed via triphenyl tetrazolium chloride
(TTC), hematoxylin-eosin (H&E), and Fluoro-Jade B
(FJB) staining. The expression levels of proteins related
to the inflammatory response, pyroptosis, and synaptic
plasticity were determined via western blotting and
immunofluorescence staining. Changes in dendrites and
spines were observed via Golgi-Cox staining.
Results. Compared with those of the tMCAO group,
the neural function scores and escape latency of the
EA+tMCAO group were reduced. The cerebral infarct
volume and the number of denatured neurons decreased.
NF-κB, caspase-1, NLRP3, and IL-18 expression levels
were significantly decreased. PSD95, SYP, and BDNF
expression levels were significantly increased. The total
number of dendrite junctions and the total length of dendrites increased. Compared with the EA+tMCAO
and NS+EA+tMCAO groups, the escape latency in the
lipopolysaccharide (LPS)+EA+tMCAO group was
significantly increased. NF-κB, IL-18, and cleaved
caspase-1 expression levels were elevated.
Conclusion. EA may inhibit NF-κB/NLRP3 pathway
proteins; regulate the neuroinflammatory response;
promote the expression of PSD-95, SYN, and BDNF;
improve the structure of dendrites and dendritic spines;
and alleviate cognitive impairment in rats with CIRI.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/