Abstract
Ischemic stroke is a common cause of morbidity, mortality, and disability worldwide. Electroacupuncture (EA) is an effective method for alleviating brain damage after ischemic stroke. However, the underlying mechanism has not been fully elucidated. This study aimed to determine whether endoplasmic reticulum stress (ERS) could contribute to the protective effects of EA in cerebral ischemia/reperfusion injury (CIRI) to provide a rationale for the widespread clinical use of EA. Rats were divided into the sham-operated (sham) group, the CIRI (model) group, and the EA group. Rats in the model group were subjected to middle cerebral artery occlusion (MCAO) for 2 h followed by 72 h of reperfusion. Rats with CIRI were treated daily with EA at GV20 and ST36 for a total of 3 days. The Longa scoring system and adhesive removal somatosensory test were applied to evaluate neurological deficits. Then, 2,3,5-triphenyltetrazolium chloride (TTC) staining was performed to measure the infarct volume. Immunofluorescence staining for NeuN and GFAP and terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP nick-end labeling (TUNEL) staining were performed to detect apoptotic cells in brain tissue. Immunohistochemistry, quantitative real-time polymerase chain reaction (qPCR), and western blotting were used to measure the levels of ERS indicators (GRP78, CHOP/GADD153, p-eIF2α, and caspase 12). The results showed that EA significantly reduced the cerebral infarct volume, improved neurological function, and inhibited neuronal apoptosis. In the EA group compared with the model group, the mRNA expression levels of GRP78 were significantly increased, and the expression levels of proapoptotic proteins (CHOP/GADD153, p-eIF2α, and caspase 12) were significantly decreased. These results suggest that the possible mechanism by which EA protects cells against neuronal injury in CIRI may involve inhibiting endoplasmic reticulum stress.
Highlights
Stroke is considered the leading cause of disability and death, and ischemic strokes account for approximately 80% of all strokes [1]
To validate the protective effect of EA treatment against cerebral ischemia/reperfusion injury (CIRI), we performed middle cerebral artery occlusion (MCAO) surgery in rats as described previously [17]. e rats were randomly divided into the CIRI model group and the EA treatment group, while the sham-operated group served as the control (Figure 1(a))
We examined the neurological deficits of rats. e results showed that the EA group exhibited significantly lower neurological deficit scores and better performance in the adhesive removal test than the model group at 72 h after reperfusion (Figures 1(d) and 1(e)). ese results demonstrated that EA could reduce cerebral infarct volume and ameliorate neurobehavioral deficits
Summary
Stroke is considered the leading cause of disability and death, and ischemic strokes account for approximately 80% of all strokes [1]. The incidence of ischemic stroke has been increasing, resulting in high healthcare costs and imposing a financial burden on both families and society [2, 3]. Intravenous tissue-type plasminogen activator (rt-PA) is the only thrombolytic drug approved by the FDA for the treatment of ischemic stroke. And successful restoration of blood supply is the most effective treatment for reducing the cerebral infarct volume. The restoration of blood flow is frequently associated with additional brain injury, which is referred to as cerebral ischemia/reperfusion injury (CIRI) [5]. Many studies have reported that apoptosis plays an important role in the pathophysiology of CIRI [7,8,9]. Recent studies have revealed that endoplasmic reticulum stress (ERS) is an essential signaling event for neuronal apoptosis resulting from CIRI [10]. Recent studies have revealed that endoplasmic reticulum stress (ERS) is an essential signaling event for neuronal apoptosis resulting from CIRI [10]. e endoplasmic reticulum (ER) is an organelle that plays a major role in the folding, posttranslational modification, and transport and secretion of lumen and membrane
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
