Electroacupuncture Regulates Endoplasmic Reticulum Stress and Ameliorates Neuronal Injury in Rats with Acute Ischemic Stroke.
Ya-Min ZhangHong XuSu-Hui ChenHua SunPublished in: Evidence-based complementary and alternative medicine : eCAM (2021)
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.
Keyphrases
- endoplasmic reticulum stress
- induced apoptosis
- cerebral ischemia
- subarachnoid hemorrhage
- acute ischemic stroke
- oxidative stress
- middle cerebral artery
- brain injury
- ischemia reperfusion injury
- blood brain barrier
- signaling pathway
- cell death
- acute myocardial infarction
- multiple sclerosis
- physical activity
- cell cycle arrest
- cardiovascular events
- atrial fibrillation
- south africa
- clinical trial
- high resolution
- internal carotid artery
- spinal cord injury
- neuropathic pain
- cell proliferation
- resting state
- coronary artery disease
- poor prognosis
- heart failure
- risk factors
- long non coding rna
- spinal cord
- percutaneous coronary intervention
- newly diagnosed