Thus, we aimed to analyze whether this flavonoid http://www.selleckchem.com/products/PD-98059.html could

be used as medicine to treat brain ischemia. We applied rutin into the acute phase of ischemia and evaluated its bioavailability and its effects on sensorimotor recovery and neurodegeneration. To evaluate whether the administration of rutin after induction of cortical ischemia results in any functional recovery, ischemic animals were treated with rutin and their sensorimotor performance was measured. In cylinder test, statistical analysis showed significant “treatment x day” interaction (F=1.56, p<0.05) and significant effects of treatment (F=3.61, p<0.05) and day (F=16.5, p<0.0001). Comparisons among groups showed more marked recovery in R50 group, and R100 showed discrete effect ( Fig. 1). Thus, rutin

promoted significant recovery of contralateral forelimb performance in support during vertical exploration. EGFR inhibitor Similarly, in adhesive test, statistical analysis showed significant “treatment x day” interaction (F=1.64, p<0.05) and significant effects of treatment (F=5.18, p<0.05) and day (F=30.19, p<0.0001). Comparisons among groups also showed more marked recovery in R50 group than in R100 group ( Fig. 2). Sham animals were also evaluated and showed no significant lost of function ( Fig. 2). Thus, rutin promoted significant recovery of adhesive removal with contralateral forelimb after tactile stimulation. Together, these results suggest that post-ischemic treatment with rutin is effective to recover sensorimotor function after cortical focal ischemia. Since the dose of 50 mg/kg showed better result, it was used in further experiments. Experiments with HPLC showed the presence of rutin in plasma from 2 h to atleast 8 h after i.p. injection, with a peak at 2–4 h (Table 1, Fig. 3). Two equations showed a close fit for obtained data, and both statistic comparisons with F test (equation (1) as the null hypothesis, F=0.09, p=0.77) and Alkaike's Information Criteria (AlCc) (% equation (1)/% equation (2)=17.24) indicated equation (1) (two phase exponential association) as the preferred model ( Table

2, Fig. 3). As previously MRIP shown (Giraldi-Guimarães et al., 2009 and Szele et al., 1995), the procedure of thermocoagulation induced a consistent ischemic lesion that included the six cortical layers, sparing the white matter as revealed by reaction with TTC (Fig. 4). Sham procedure induced no recognizable lesion (Fig. 4). Treatment with rutin promoted no significant reduction of ischemic lesion volume (p=0.65, Figs. 4 and 5). As previously shown (Giraldi-Guimarães et al., 2009), the procedure of thermocoagulation induced large neurodegeneration, as revealed by FJC staining. The majority of FJC+ cells were observed in the core of the lesion (not shown), but a significant number of stained cells was also observed in the periphery of the lesion (Fig. 6).