Extracorporeal shock wave therapy effectively protects brain against chronic cerebral hypo-perfusion-induced neuropathological changes.
Year: 2017
Type: article
Abstract: ) on day 5, 10 and 15 after CHP induction]. By day 60 after CHP induction, the white matter lesion, protein expressions of inflammatory (TNF-α/NF-κB/iNOS), oxidative-stress (NOX-1/NOX-2/NOX-4/nitrotyrosine), angiogenesis (eNOS/CD31), apoptotic (Bax/caspase-3/PARP), fibrotic (Smad3/TGF-ß) and mitochondrial-damaged (cytosolic cytochrome-C) biomarkers were significantly higher in group 2 than in groups 1 and 3, and significantly higher in group 3 than in group 1, whereas the protein expressions of anti-apoptotic (Bcl-2), anti-fibrotic (BMP-2/Smad1/5), and mitochondrial-integrity (mitochondrial cytochrome-C) biomarkers showed an opposite pattern to inflammation among the three groups (all P<0.0001). The cellular expressions of inflammatory (Iba-1/GFAP/CD14, F4/80), apoptotic (TUNEL-assay) and brain-damaged (γ-H2AX/AQP4) biomarkers showed an identical pattern to inflammation, whereas the cellular expressions of endothelial-cell (CD31/vWF), neuron/energy-integrity (NeuN/PGC-1α) and small-vessel density exhibited an opposite pattern to inflammation among the three groups (all P<0.0001). Cellular angiogenesis (VEGF/SDF-1α) significantly and progressively increased from groups 1 to 3 (all P<0.0001). In conclusion, ECSW therapy enhanced angiogenesis, inhibited molecular-cellular perturbations, and protected the white matter and neuron from CHP damage.
Source: Europe PMC (PubMed Central)
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2973899892