Bacopa monniera ameliorates cognitive impairment and neurodegeneration induced by intracerebroventricular-streptozotocin in rat: behavioral, biochemical, immunohistochemical and histopathological evidences

• DOI: 10.1007/s11011-014-9593-5
• Publication Date: 2014-07-18T03:36:20Z
• Authors: M. Badruzzaman Khan; Muzamil Ahmad; Saif Ahmad; Tauheed Ishrat; Kumar Vaibhav; Gulrana Khuwaja; Fakhrul Islam
• Keywords: Male; 0301 basic medicine; Glutathione Peroxidase; Plant Extracts; Drug Evaluation, Preclinical; Nerve Tissue Proteins; Neurodegenerative Diseases; Catalase; Hippocampus; Antioxidants; Rats; 3. Good health; Disease Models, Animal; 03 medical and health sciences; Animals; Bacopa; Lipid Peroxidation; Cognition Disorders; Energy Metabolism; Maze Learning; Glutathione Transferase; Injections, Intraventricular; Phytotherapy

The standardized extract of Bacopa monniera (BM) is a complex mixture of ingredients with a uniquely wide spectrum of neuropharmacological influences upon the central nervous system including enhanced learning and memory with known antioxidant potential and protection of the brain from oxidative damage. The present study demonstrates the therapeutic efficacy of BM on cognitive impairment and oxidative damage, induced by intracerebroventricular injection of streptozotocin (ICV-STZ) in rat models. Male Wistar rats were pre-treated with BM at a selected dose (30 mg/Kg) given orally for 2 weeks and then were injected bilaterally with ICV-STZ (3 mg/Kg), while sham operated rats were received the same volume of vehicle. Behavioral parameters were subsequently monitored 2 weeks after the surgery using the Morris water maze (MWM) navigation task then were sacrificed for biochemical, immunohistochemical (Cu/Zn-SOD) and histopathological assays. ICV-STZ-infused rats showed significant loss in learning and memory ability, which were significantly improved by BM supplementation. A significant increase in thiobarbituric acid reactive species and a significant decrease in reduced glutathione, antioxidant enzymes in the hippocampus were observed in ICV-STZ rats. Moreover, decrease in Cu/Zn-SOD expression positive cells were observed in the hippocampus of ICV-STZ rats. BM supplementation significantly ameliorated all alterations induced by ICV-STZ in rats. The data suggest that ICV-STZ might cause its neurotoxic effects via the production of free radicals. Our study demonstrates that BM is a powerful antioxidant which prevents cognitive impairment, oxidative damage, and morphological changes in the ICV-STZ-infused rats. Thus, BM may have therapeutic value for the treatment of cognitive impairment.