Electroacupuncture improves post-traumatic stress disorder in rats by alleviating hippocampal mitochondrial injury via regulating Bcl-2/Bax/caspase-3 signaling.
10.12122/j.issn.1673-4254.2025.11.10
- Author:
Dandan MA
1
;
Jie CHENG
1
;
Hong ZHANG
1
;
Guang LIU
1
;
Kai SONG
2
Author Information
1. College of Acupuncture and Tuina, Chengdu University of Traditional Chinese Medicine, Chengdu 610000, China.
2. Sichuan Health and Rehabilitation Vocational College, Zigong 643000, China.
- Publication Type:Journal Article
- Keywords:
anxiety disorder;
caspase-3;
electroacupuncture;
mitochondria;
neurons;
post-traumatic stress disorder
- MeSH:
Animals;
Electroacupuncture;
Stress Disorders, Post-Traumatic/metabolism*;
Hippocampus/pathology*;
Rats, Sprague-Dawley;
Male;
Rats;
Mitochondria/pathology*;
Signal Transduction;
bcl-2-Associated X Protein/metabolism*;
Caspase 3/metabolism*;
Proto-Oncogene Proteins c-bcl-2/metabolism*;
Disease Models, Animal
- From:
Journal of Southern Medical University
2025;45(11):2375-2384
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the mechanism underlying the therapeutic effect of electroacupuncture (EA) on post-traumatic stress disorder (PTSD) in rats.
METHODS:Forty male SD rats were randomized equally into blank control group, PTSD model group, sham-acupuncture group, paroxetine group, and EA group. In the latter 3 groups, the rat models of PTSD, induced by continuous single-prolonged stress and plantar electrical stimulation, were treated with EA at GV20, GV24, BL18 and BL23 acupoints for 15 min (5 times a week for 3 weeks), sham-acupuncture without electrical stimulation, or gavage with paroxetine suspension on the same schedule. Behavioral changes of the rats were evaluated using open field test (OFT) and elevated plus maze (EPM) test. Hippocampal pathologies and neuronal changes were examined with HE and Nissl staining, and mitochondrial ultrastructure was examined using electron microscopy. The mRNA and protein expression levels of Bcl-2, Bax, and caspase-3 were detected by RT-qPCR and immunofluorescence staining.
RESULTS:The rat models of PTSD showed significantly reduced total distance traveled in OFT and distance and time spent in the open arms of the EPM, with decreased hippocampal neurons, obvious neuronal and mitochondrial pathologies, decreased hippocampal expression of Bcl-2, and increased Bax and caspase-3 expressions. Treatments with paroxetine and EA both significantly improved behavioral changes of the rat models, increased the number of Nissl-stained neurons, obviously alleviated pathologies in the hippocampal neurons and mitochondrial ultrastructure, increased hippocampal Bcl-2 expression, and lowered caspase-3 expressions. Paroxetine showed significantly better effect than EA for improving performance of the rats in EPM test, whereas sham-acupuncture did not produce any significant improvement.
CONCLUSIONS:EA alleviates PTSD in rats possibly by upregulating Bcl-2 and downregulating Bax and caspase-3, thereby ameliorating hippocampal mitochondrial damage.
