Brain-targeting form of @entity4600 for experimental XXXX treatment: MRI evaluation and anti-oxidant impact.

@entity64 @entity6579 @entity4600 @entity2500 @entity4601 @entity10329 @entity9539 @entity35
Epidemiologic studies report cardiovascular protection conferred by @entity9539 , in particular @entity4600 ( @entity4601 ). However, few experimental studies have addressed its potential in @entity64 treatment. The present study used multimodal MRI to assess in vivo the neuroprotection conferred by @entity4601 and by a brain-targeting form of @entity4601 -containing @entity6579 (AceDoPC) in experimental @entity64 . @entity35 underwent intraluminal @entity2500 ( @entity2500 ) and were treated at reperfusion by intravenous injection of i) saline, ii) plasma from donor @entity35 , iii) @entity4601 or iv) AceDoPC, both solubilized in plasma. Twenty-four hours after reperfusion, animals underwent behavioral tests and were sacrificed. Multiparametric MRI (MRA, DWI, PWI, T2-WI) was performed at H0, during occlusion, and at H24, before sacrifice. Brain tissue was used for assay of F(2)- @entity10329 as lipid peroxidation markers. Initial lesion size and PWI/DWI mismatch were comparable in the four groups. Between H0 and H24, lesion size increased in the saline group (mean    s.d.: +18%    20%), was stable in the plasma group (-3%    29%), and decreased in the @entity4601 (-17%    15%, P=0.001 compared to saline) and AceDoPC (-34%    27%, P=0.001 compared to saline) groups. Neuroscores in the AceDoPC group tended to be lower than in the other groups (P=0.07). Treatments (pooled @entity4601 and AceDoPC groups) significantly decreased lipid peroxidation as compared to controls (pooled saline and vehicle) (P=0.03). MRI-based assessment demonstrated the neuroprotective effect of @entity4601 in the @entity2500 model. Results further highlighted the therapeutic potential of engineered brain-targeting forms of @entity9539 for @entity64 treatment.
