Tannic Acid Attenuates Quinolinic Acid-Induced Neurodysfunction by Modulating Oxidative Stress Parameters and Electrogenic Pump Activity

Abstract The pathophysiology of neurodegenerative illnesses is largely dependent on oxidative stress and poor ion homeostasis, and these conditions represent a substantial worldwide health burden. Endogenous neurotoxic quinolinic acid (QA) is linked to neurodysfunction by inducing oxidative stress and interfering with sodium pump function. In a number of models, the polyphenolic molecule tannic acid (TA), which has strong antioxidant qualities, has demonstrated pharmacological effects in several diseased conditions. However, the neuroprotective effect of TA is rather speculative and still very open for clarification. In the present study, an in vitro model was employed to examine the effect of TA on deoxyribose degradation, lipid peroxidation, thiol status, antioxidant enzymes and cerebral and spinal sodium pump in rat cerebral and spinal tissue homogenates treated with quinolinic acid (QA, 2 mM). Results revealed that QA treatment led to a profound (p < 0.05) degradation of deoxyribose, formation of thiobarbituric acid reactive substances (TBARS), and marked (p < 0.05) reduction in tissue level of free thiols. However, TA treatment significantly (p < 0.05), counteracted TBARS production, deoxyribose degradation and markedly (p < 0.05) increased the thiol level of the cerebral and spinal tissue homogenates. Furthermore, QA markedly (p < 0.05) diminished the activities of cerebral and spinal antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD), Glutathione Peroxidase (GPx) and Glutathione S transferase (GST)] and impaired the activities of cerebral and spinal sodium pump. Nonetheless, the activities of the antioxidant enzymes and pump were all raised in both the cerebral and spinal tissue homogenates upon TA treatment. These findings justify the pharmacological action of TA on QA-induced neurotoxicity and suggest its potential use in the treatment of neurodegenerative diseases. Further investigation is required to determine TA's translational usefulness in clinical settings.