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Neurological deficit was assessed at D1 and pMCAo mice were compared to nonoperated mice, before randomization into the three groups.
Infarct volume was assessed three days after pMCAo, on coronal 30 [micro]m sections stained with cresyl violet.
At D1, we observed a significant reduction in the neurological score in operated (pMCAo) compared to nonoperated mice (33.1 [+ or -] 3.0 versus 36 [+ or -] 1.0, resp., P <0.001).
Fourth, the known rapid recovery of C57Bl6J mice subjected to pMCAo, particularly when the infarct is small, prevented us from showing any significant differences between PB-MNC+ and PB-MNC-treated mice on the neurological score assessment or the ink test.
In vivo, baicalin was found to reduce neurological deficit scores and cerebral infarct volume of Sprague-Dawley rats after pMCAO .
Wogonin was found to reduce the total infarction volume and improve the behavioral deficits in rats after pMCAO .
CSF was collected by cisternal puncture when the animals were killed at either 2 h [sham (n = 4), pMCAO (n = 5), tMCAO (n = 3)] or 24 h [sham (n = 5), pMCAO (n = 4), tMCAO (n= 3)] postsurgery.
The concentration [mean (SE)] of VLP-1 in the CSF of pMCAO rats was higher [16.8 (6.5 [micro]g/L)] than in tMCAO [6.0 (2.4 [micro]g/L)], although the difference was not statistically different (P = 0.23, unpaired t-test).
The STVNA therapeutic window was investigated at a single dose of 10 mg/kg in both transient (tMCAO) and permanent (pMCAO) ischemia models.
In the current study, we demonstrated the dose-response relationship and defined the therapeutic window for the neuroprotective effects of STVNA in tMCAO and pMCAO. The presented data show that moderate doses of STVNA (5, 10, and 20 mg/kg) have a protective effect against neuronal damage induced by cerebral ischemia and that this protection is associated with an improvement in neurological functions.
Caption: Figure 5: Effects of STVNA treatment in pMCAO. (a) The infarct volume of each group 24 hours after pMCAO.
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