After predetermined time point of I/R, the brains were quickly removed and sliced into coronal sections of 2 mm thickness. Each slice was immersed in a 1.0% solution of 2,3,5-triphenyltetrazolium chloride (TTC) for 30 min. Necrotic infarcted tissue was unstained and viable tissue was stained dark red, further separated, weighed and percentage of infarction was determined.19 The stained tissue was not suitable for estimating oxidative and inflammatory biomarkers; hence a separate group of animals were used for estimating the levels of these biochemical parameters (Table 2). The brain tissue of each animal was removed after completion of 4 h reperfusion and used for the estimation of superoxide

dismutase (SOD), catalase (CAT), myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). SOD Tyrosine Kinase Inhibitor Library concentration levels were determined by the method developed by Kakar

et al.20 CAT levels were determined by the method developed by Aebi et al21 MDA levels were determined by the method developed by Ohkawa et al22 MPO levels were determined by the method developed by Mullane et al23 TNF-α levels were determined by using AssayMax Rat Tumor Necrosis Factor-alpha (TNF-alpha) ELISA Kit (Catalog No. ERT2010-1).24 IL-10 levels were determined by using Apoptosis Compound Library AssayMax Rat Interleukin-10 (IL-10) ELISA Kit (Catalog No. ERI3010-1).25 Statistical analysis was performed using Prism software (Version 6.02). Results of percentage of infarct size are shown in Table 3 and Fig. 2 and Fig. 3. Cerebral Infarct because size was found to be 48.34 ± 0.84% in rats subjected to cerebral I/R injury. Significant cerebral damage was observed in I/R control group animals when compared to sham operated group. Pyrimidines (AUCP1 and AUCP2) treatment offered dose dependent cerebroprotection in terms of significant reduction in cerebral infarct size when compared to I/R control group. AUCP2 has offered more degree of cerebroprotection when compared to AUCP1. Results of tissue SOD levels are shown in Table 4 and Fig. 4. Results shown in the above mentioned figure indicate that the cerebral ischemia

and reperfusion significantly decreased antioxidant enzyme (SOD) levels in the injured brain tissue of rats as compared with the sham control group. Results of tissue SOD levels are shown in Table 4 and Fig. 5. Results shown in the above mentioned figure indicate that the cerebral ischemia and reperfusion significantly decreased antioxidant enzyme (CAT) levels in the injured brain tissue of rats as compared with the sham control group. Results of tissue MDA levels are presented in Table 4 and Fig. 6. Results shown in the above mentioned figure indicate that the cerebral ischemia and reperfusion significantly increased lipid peroxidation (MDA) levels in the injured brain tissue of rats as compared with the sham control group. Results of tissue MPO levels are presented in Table 4 and Fig. 7.