Objective: To clarify the effects of repetitive transcranial magnetic stimulation (rTMS) on rat motor cortical excitability and neurofunction after cerebral ischemia-reperfusion injury.
Methods: After determined awake resting motor threshold (MT) and motor evoked potentials (MEPs) of right hindlimbs, 20 Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) reperfusion injury, then rTMS were applied to rTMS group (n=10) at different time, while control group (n=10) received no stimulation. A week later, MT and MEPs were evaluated again, as well as neurological deficits and infarct volume. The effects of rTMS and MCAO reperfusion injury on these parameters were analyzed.
Results: After MCAO reperfusion, both MT level and neurological deficit scores increased, distinct focal infarction formed, and latency of MEP elongated. Compared with the control group, the increased extent of MT and neurological scores of rats receiving rTMS were significantly lower (P < 0.05), as well as the infarct volumes reduced significantly (P < 0.05). But MEP was not affected by rTMS obviously. There was a positive linear correlation between postinjury MT and infarct volume (r = 0.64, P < 0.05).
Conclusion: rTMS may facilitate neurofunction recovery after cerebral ischemia-reperfusion. Postinjury MT could provide prognostic information after MCAO reperfusion injury.
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J Stroke Cerebrovasc Dis
January 2025
Department of Gerontology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, 646000, China. Electronic address:
Objective: Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway.
Methods: An in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs).
Neuroimage
December 2024
F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute, Baltimore, MD, USA; Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address:
This study aims to investigate the variations in guanidino (Guan), amine and amide chemical exchange saturation transfer (CEST) contrasts in ischemic stroke using permanent middle cerebral artery occlusion (pMCAO) and transient MCAO (tMCAO) models at high (9.4T) and clinical (3T) MRI fields. CEST contrasts were extracted using the Polynomial and Lorentzian Line-shape Fitting (PLOF) method.
View Article and Find Full Text PDFJ Mol Histol
December 2024
The Second Clinical Medical College, Southern Medical University, Guangzhou City, Guangdong Province, 510515, China.
This study was to investigate the role of microRNA (miR)-330-5p derived from mesenchymal stem cells-secreted exosomes (MSCs-Exo) in cerebral ischemia-reperfusion injury (CI/RI) through targeting lysine N-methyltransferase SET domain containing 7 (SETD7). MSCs-Exo were separated and identified. MSCs-Exo were used to treat the middle cerebral artery occlusion (MCAO) rat model.
View Article and Find Full Text PDFJ Ethnopharmacol
December 2024
Xi'an Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Medical Research, Northwestern Polytechnical University, 127 West Youyi Road, Xi'an, Shaanxi, 710072, China. Electronic address:
J Integr Neurosci
December 2024
Department of Neurology, Hainan West Central Hospital, 571799 Danzhou, Hainan, China.
Background: Ischemic stroke (IS) is the leading cause of mortality worldwide. Herein, we aimed to identify novel biomarkers and explore the role of C-type lectin domain family 7 member A () in IS.
Methods: Differentially expressed genes (DEGs) were screened using the GSE106680, GSE97537, and GSE61616 datasets, and hub genes were identified through construction of protein-protein interaction networks.
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