نبذة مختصرة : It is well known that inflammatory reactions and oxidative stress play a key role in the pathogenesis of cerebral ischemia and secondary injury. Boeravinone B (BB) proofed their anti-inflammatory and antioxidant effect, but their neuroprotective effects still unknown. In this experimental study, we explore the neuro-protective effect of Boeravinone B on the ischemia/reperfusion and explore the possible mechanism. Male Wistar rats were used for the current experimental study. First induces natural I/R injury in rats and treated with BB and nifedipine, respectively. Rats were subjected to ischemia after 6 consecutive days by occlusion of the bilateral common carotid arteries (BCCAO). Neurological score, biochemical, antioxidant, pro-inflammatory cytokines and inflammatory parameters were estimated in the serum and brain tissue. BB treatment significantly (p < 0.001) suppressed neuronal injury, dose-dependently decreased the cerebral water content. BB treatment altered the pro-inflammatory cytokines, antioxidant and inflammatory mediators in the serum and brain tissue. BB regulated the expression of glycine (Gly), glutamic acid (Glu), taurine (Tau), aspartic acid (Asp) and γ-aminobutyric acid (GABA) and enhanced the activity of Na+, K+ ATPase and Ca2+ ATPase. BB significantly (p < 0.001) reduced antioxidant enzymes such as glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), malondialdehyde (MDA), glutathione reductase (GR); inflammatory cytokines include interleukin-4 (IL-4), interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-6 (IL-6) and interleukin-1β (IL-1β); inflammatory mediators include prostaglandin (PGE2), nuclear kappa factor B (NF-κB) and cyclooxygenase-2 (COX-2), respectively. In this study, we have found that Boeravinone B exhibited protection against cerebral I/R by reducing oxidative stress and inflammatory reaction.
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