Search

Objective: To assess the effectiveness of electroacupuncture (EA) with rehabilitation training in reducing limb spasticity in post-stroke patients., Methods: A systematic review was performed by electronically searching six databases (Medline/Pubmed, Embase, Cochrane Library, China National Knowledge Infrastructure, Database for Chinese Technical Periodicals, and Wanfang Data) for randomized controlled trials (RCTs) on EA with rehabilitation training for limb spasticity reduction in post-stroke patients from 1 January 2009 to 1 January 2019. A meta-analysis was performed using SAS 9.3 and RevMan 5.3 software after bibliography screening, data extraction, and risk of bias assessment using the Cochrane handbook. The primary outcome was spasticity., Results: A total of 31 RCTs (including 2488 participants) were included. Except for Cai et al.'s study, the quality of other RCTs was not high. All studies performed a descriptive analysis, and 29 RCTs conducted a meta-analysis. The odds ratio (OR) for marked efficiency was 2.35 (95% confidence interval [CI] 1.68-3.27, Z = 5.03, P < .00001). The OR for Modified Ashworth Scale (MAS) classification was 2.42 (95% CI 1.89-3.10, Z = 7.03; P < .00001). The weighted mean difference (WMD) for MAS score was -0.68 (95% CI -0.79 - -0.56, Z = 11.24, P < .00001). The WMD for clinical spasticity index score was -1.50 (95% CI -2.28 - -0.72, Z = 3.79, P = .0002)., Conclusion: EA with rehabilitation training could be a good strategy for reducing limb spasticity after stroke and is better than EA alone or rehabilitation training alone. However, its effectiveness remains to be further verified by large-sample and high-quality RCTs.

Background: Electroacupuncture (EA) pre-treatment can play a significant neuroprotective role in rats with cerebral ischaemia and reperfusion (CIR) injury, but the specific mechanism needs to be further elucidated. Objective: To investigate the effects of EA pre-treatment on apoptosis-related proteins Bax, Bcl-2, Cytochrome c (cyt c), cleaved caspase-9 and -3 in rats with CIR injury. Methods: CIR injury was induced using middle cerebral artery occlusion (MCAO) ischaemia-reperfusion. Thirty-six male Specific Pathogen Free (SPF) Sprague-Dawley rats were randomly divided into three groups: Sham (n=12), MCAO (n=12), and the EA+MCAO group (n=12). EA+MCAO group rats received electroacupuncture at DU20 for 2 consecutive weeks before MCAO model preparation. After 24 h of reperfusion, neurological deficits were evaluated by modified neurological severity scores. Brain infarct volumes were examined by 2,3,5-triphenyltetrazolium chloride staining. Expression of Bax, Bcl-2, cyt c, cleaved caspase-9 and -3 in the ischaemic penumbra were detected by Western blotting, and apoptosis evaluated by TUNEL staining. Results: After perfusion for 24 h, compared with the MCAO group, the neurological deficit scores and brain infarct volumes in the EA+MCAO group were significantly decreased (P <0.05), as was the level of Bax (P <0.05) or the Bax/Bcl-2 ratio (P <0.05), levels of cyt c, cleaved caspase-9 and -3 also decreased (P <0.05), like the number of TUNEL-positive cells (P <0.05), in contrast, the level of Bcl-2. Conclusion: EA pre-treatment exerts an anti-apoptotic effect through Bax-to-Bcl-2 ratio downregulation, blockage of mitochondrial cyt c release to the cytosol, and reduction of caspase-9 and -3 expression in rats with CIR injury. [ABSTRACT FROM AUTHOR]

In recent years, the efficacy of electroacupuncture (EA) pretreatment generating ischemic tolerance mimicking ischemic pretreatment (IP) has been continuously confirmed, which was first found in the brain and then in the heart. Furthermore, researchers have observed the intensive cardioprotection impact of EA pretreatment on patients undergoing percutaneous coronary intervention (PCI) and heart valve replacement, indicating that EA pretreatment tends to be a valuable and advantageous avenue for preventing acute myocardial ischemia/reperfusion (I/R) injury or treatment of ischemic heart disease (IHD). In reality, the heart protection mechanism of EA pretreatment is robust and pleiotropic, of which the regulatory molecular pathways are involved in multichannel, multilevel, and multitarget, including energy metabolism, inflammatory response, calcium overload, oxidative stress, autophagy, and apoptosis. Through a growing number of clinical tests and basic experiments with animal models, researchers progressively explored the optimal acupoints and parameters, where EA pretreatment induced acute and delayed ischemic tolerance for myocardial protection. Thereby, this article aims to collect the relevant evidence on EA pretreatment against myocardial ischemia/reperfusion injury (MIRI) and summarize the mechanism of cardioprotection of EA pretreatment to provide ideas and methods for further clinical applications. [ABSTRACT FROM AUTHOR]