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Subject: Veterinary Pharmacology and Toxicology × End date: 2017 × Start date: 2017 ×
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    ThesisItemOpen Access
    STUDIES ON THE THERAPEUTIC POTENTIAL OF A FEW MEDICINAL PLANT EXTRACTS AS MEMORY ENHANCERS ON EXPERIMENTALLY INDUCED COGNITIVE DYSFUNCTION IN LABORATORY ANIMAL MODELS
    (Assam Agricultural University, Khanapara, Guwahati, 2017-07) SAIKIA, BEENITA; Barua, Chandana Choudhury
    The present study was undertaken to explore the cognition-enhancing activity of different extracts of few medicinal plants. Ethanol, hydroethanol, aqueous, petroleum ether, n- hexane, ethyle acetate and chloroform extracts of seeds of Zanthoxylum alatum and leaves of Conyza bonariensis were experimentally used to treat scopolamine-induced amnesia in rats and mice. Four (4) different models, universally used for learning and memory studies, were utilized in the present study, i.e., Elevated plus maze (EPM) and Morris water maze (MWM) in mice, Radial arm maze (RAM) and Barnes maze (BM) in rats. The study was targeted to develop plant-based anti-amnesic agents. Preliminary behavioural studies were performed for all the extracts using Morris water Maze. Hydroethanolic extract of Z. alatum (HEZA) and petroleum ether extract of C. bonariensis (PECB) were found to be more active than other extracts. The extracts were further subjected to detailed biochemical and molecular analyses in order to assess their mechanism of action. The animals were divided into nine (9) groups, each consisting of 6-10 numbers of animals. Tacrine (3 mg/kg; intra-peritonial) was used as standard nootropic drug. Scopolamine (0.4 mg/kg, intra-peritonial) was used to produce amnesia. Phytochemical studies revealed that HEZA contains terpenoids, tannins and saponins; whereas PECB contains alkaloids, flavonoids, terpenoids, saponins and glycosides. HEZA and PECB exhibited cognition-enhancing activity as indicated by a significant reduction in the transfer latency (TL) and increased in inflexion ratio (IR), in the EPM. Likewise, reduction in escape latency (EL) and path length and increased time spent in target quadrant (TSTQ) in MWM; decreased WME (working memory error) and RME (reference memory error) in RAM; decreased escape latency (EL) in BM, indicated protection from loss of memory after treatment with HEZA and PECB. Standard drug tacrine showed similar result. Pretreatment with standard drug tacrine and test drug HEZA and PECB significantly decreased the AChE activity and also prevented scopolamine-evoked oxidative stress by improving reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and decreasing lipid peroxidation (LPO) and nitrite (NO) level. HEZA and PECB also inhibited the scopolamine-induced β amyloid accumulation and pro-inflammatory cytokines (TNF-α, IL-1β) and also significantly increased the anti-inflammatoty cytokine (IL-10). HEZA and PECB also significantly increased the mRNA expression of Nrf2, HO-1, PP2A and decreased the mRNA expression of AChE, Tau, NFκB in the hippocampus of mice and rats. The same results were also observed after treatment with tacrine, when compared with scopolamine-treated animals. The immunoblotting assay showed significant up regulation of BDNF and TrkB protein expression with simultaneous down regulation of caspase-3 and Bax protein expression in the hippocampal tissues of mice and rats similar to tacrine, as compared with scopolamine treated group. In conclusion, HEZA & PECB exhibit multiple pathways for cognition enhancement in scopolamine-induced amnesia in mice and rats. The mechanism by which HEZA & PECB performs anti-amnesic activity could be through inhibition of the key enzymes AChE, preventing Tau aggregation, impending neuro-inflammation, increase BDNF level and its antioxidants property. HEZA showed more potency than PECB in cognition enhancement where as tacrine, showed the best activity in all the models comparable to Z. alatum. Therefore, it might be suggested that these two test plants might go a long way in the management of cognitive dysfunctions in human and animal subject. However, further studies are required to isolate the active compounds responsible for cognition-enhancing property.