Pericyte protection by edaravone after tissue plasminogen activator treatment in rat cerebral ischemia.
Bottom Line: Thus, tPA treatment damaged pericytes, resulting in the detachment from astrocytes and a decrease in glial cell line-derived neurotrophic factor secretion.However, treatment with edaravone greatly improved tPA-induced damage to pericytes.The present study demonstrates that exogenous tPA strongly damages pericytes and destroys the integrity of the NVU, but edaravone treatment can greatly ameliorate such damage after acute cerebral ischemia in rats.
Affiliation: Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.Show MeSH
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Mentions: Color panels in Figure 1 show the peri-ischemic brain regions. PDGFRβ-positive pericyte (red) partially overlapped (merged, yellow) with NAGO-positive endothelial cells (green). The coverage of PDGFRβ-positive pericytes with NAGO-positive endothelial cells was significantly reduced at 1 day after tMCAO (54.0% ± 2.2%, P < 0.01 vs. SC) compared with that of SC (61.7% ± 2.7%) and then increased significantly at 4 days (69.9% ± 1.3%, P < 0.01 vs. SC; Fig. 1B).
Affiliation: Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.