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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: Stroke. 2017 Jun 6;48(7):1948–1956. doi: 10.1161/STROKEAHA.117.016474

Figure 6. MRE-269 reduced BBB damage and MMP-9 activity in aged rats following transient MCAO.

Figure 6

A) Ischemic stroke significantly increased BBB permeability as assessed by IgG extravasation, and treatment with MRE-269 (0.25 mg/kg; i.v.) at 4.5h after stroke onset significantly reduced the IgG extravasation into the ipsilateral cerebral cortex compared to vehicle rats. B) Activation of matrix metalloproteinase (MMP)-9 is a key pathological mechanism in stroke leading to BBB breakdown. Administration of MRE-269 (0.25 mg/kg; i.v.) significantly reduced stroke-induced MMP-9 activity in the ipsilateral cerebral cortex compared to vehicle group. Data were expressed as mean ± SEM, *P<0.05, ***P<0.001 versus sham ipsilateral and #P<0.05 versus vehicle ipsilateral. Sham, n=5; Vehicle, n=12; MRE-269, n=13. CXI = cortex ipsilateral to stroke; CXC = cortex contralateral to stroke.