Memory disorders are the progressive neurological disorder, mainly causing dementia, memory loss and cognitive dysfunctions. The current study is aimed to experimentally validate the crude extract of Canna indica aerial parts (CIA) and root (CIR) against aluminium chloride induced altered memory in rats. Initially, methanolic extract of CIA, hydroalcoholic extract of CIR, and their combination of CIA + CIR were screened for Invitro antioxidant activity via 2,2-diphenyl-1-picrylhydrazyl (DPPH) and nitric oxide (NO) assays, acetylcholinesterase (AChE) inhibitory assay and were also screened for their memory enhancing activity by in-vivo models such as elevated plus maze (EPM), morris water maze (MWM), cooks pole climb (CPC), Actophotometer, novel object recognition (NOR), and T-maze. Aluminium chloride (AlCl 3 ) (17 mg/kg/day p.o.) for 21 days, was used as an Alzheimer's disease inducing agent and Donepezil (AChE inhibitor) as a standard treatment agent. The AChE, butyrylcholinesterase (BChE) activity and malondialdehyde (MDA) level were significantly increased, and glutathione (GSH), total protein (TP), catalase (CAT), and Dopamine were decreased only in AlCl 3 treated rats and treatment with CIA 200 mg/kg and CIA + CIR 200 mg/kg significantly reversed these mechanisms.Histopathology of cortex and hippocampus was examined at 40× magnification, indicating maintain of integrity and architecture of CA1 and CA3 neuronal cells compared to control and standard groups. The in vivo studies of interospective and exteroceptive behavior models (EPM), MWM, CPC, Actophotometer, NOR, T-maze revealed that AlCl 3 administration enhanced transfer latency (TL), escape latency time (ELT) and decreases locomotion, discriminatory index, and percentage alternation respectively. However, treatment with CIA and CIA + CIR 200 mg/kg highly significantly reversed the pathological changes of disease, extracts of Canna indica of both root and aerial parts phyto constituents are rich in flavonoids, phlobatannins, anthocyanin pigments, saponins, alkaloids, steroids, terpenoids etc. Which will decipher the acetylcholinestrase inhibitory, antioxidant and antiinflammatory activity, will ameliorate the pathological state of Alzheimer disease.

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The present study is aimed to evaluate the effect of ylang ylang essential oil in alcohol induced hepatotoxicity in rats. Alcohol was used as an inducing agent and Silymarin as a standard molecule. Body weight was measured at a 3 days interval till the twenty first day and at the end of the study, serum AST, ALT, TP, TC, TG, and TB biomarkers were estimated. Further, the liver tissue was evaluated for antioxidant enzymes namely CAT, LPO, SOD and GSH level. Liver weight and histopathology was accessed at the end. Phytocompounds were shortlisted from literature and curated databases. Probable targets of each compound were identified using the SwissTargetPrediction web server. Probable mechanisms of phytocompounds against Alcohol induced hepatotoxicity were analyzed by the STRING and KEGG pathway database. The network between compounds, targets, and pathways was generated via Cytoscape ver. 3.6.1. Docking was performed by AutoDock vina using PyRx0.8v. YYEO group showed increased BW compared to alcohol group and also reversed the increased serum AST, ALT, TP, TC, TG, and TB biomarkers and also increased the level of antioxidant enzymes compared to alcohol induced group. YYEO 400 mg/kg exhibited normal liver weight and histology compared to alcohol. Enrichment and network analysis identified YYEO 63 compounds as beneficial modulators of protein molecules associated with hepatotoxicity via modulating Toll-like receptor, Adipocytokine, TNF, Sphingolipid, FoxO, AMPK, Relaxin, MAPK, NF-kappa B, HIF-1, Fc epsilon RI, IL-17, VEGF, T cell receptor, NOD-like receptor, mTOR, PI3K- Akt signaling pathway, etc. Canangaterpene 1 was identified as a potent inhibitor of aldose reductase. Graphical abstract