Vanillic Acid Improve Neural Function after Focal Cerebral Ischemia-reperfusion Rats

Background and Objective: Vanillic Acid (VA) is a dihydroxybenzoic acid derivative found in in the roots of Angelica sinensis and used for treating various ailments. The current preclinical study was designed to demonstrate the neuroprotective activity of VA against cerebral Ischemia-Reperfusion (I/R) injured rat model. Materials and Methods: Healthy Sprague-Dawley (SD) rats (n = 40) were segregated into 4 groups. Rats received only saline (Group I), rats were induced by Middle Cerebral Artery Occlusion (MCAO) for 90 min and followed by reperfusion for 24 h (group II), group III and IV rats pretreated with VA (50 or 100 mg kg(-1)) for 14 days and followed by MCAO induction. Data were analyzed using Turkey's test with SPSS software. Results: A considerable decline in the neurological deficit score and cerebral infarct area was observed in VA pretreated group. On administration with VA (50 or 100 mg kg(-1)) concomitantly lowered the levels of lipid peroxidation product (Malondialdehyde-MDA) with improved antioxidant status (superoxide dismutase, catalase). Whereas, the inflammatory markers such as interleukins-6 (IL-6), IL-1 beta, Tumor Necrosis Factor Alpha (TNF-alpha) and Nuclear Factor Kappa B (NF-kappa B) p65 subunit were remarkably decreased upon VA supplementation, on comparison with MCAO induced group. Furthermore, the relative protein expression of TNF-alpha and NF-kappa B p65 were significantly hampered on 14-day intervention with VA. Conclusion: The outcome of this study inferred that VA (100) could exert better neuroprotective activity by improving neuronal function via attenuating inflammatory cascade.