Original Article Chemical Profiling and Dose-Dependent Assessment of Fear Reducing and Memory-Enhancing Effects of Solanum virginianum in Rats Usman Javaid 1 , Sana Javaid 1,2 , Waseem Ashraf 1 , Muhammad Fawad Rasool 3 , Omar M. Noman 4 , Ali S. Alqahtani 4 , Abdul Majeed 3 , Waleed Shakeel 1 , Thamer H. Albekairi 5 , Faleh Alqahtani 5 , and Imran Imran 1 Abstract The current study was planned to investigate the pharmacological basis of Solanum virginianum extract (SV.CR) pertaining to anxiolytic, antidepressant and memory-enhancing effects in rats. The SV.CR was analyzed in-vitro for phytoconstituents, anti- oxidant potential and anticholinesterase activity. The rats treated in a dose-dependent manner (25, 50 and 100 mg/kg of SV.CR) were subjected to behavioral tests for anxiety, depression and memory judgment followed by biochemical studies. A notable dose-dependent anxiolytic potential of SV.CR was observed in elevated plus maze and open field tests (P < 0.05). The decreased immobility time of the treated rats in the forced swim test (P < 0.01) unveiled the plant’s potential to reduce depression. Moreover, SV.CR treatment also reversed scopolamine-impaired cognition (P < 0.05) in various deployed memory and learning tasks. Biochemical studies of brain homogenates of SV.CR treated animals demonstrated decreased anticholinesterase activity and lipid peroxidation levels whereas increased levels of superoxide dismutase and glutathione peroxidase (P < 0.05 vs scopolamine group) were noted. The scientific validation of the study supported the use of Solanum virginianum in reducing anxiety, depression and amnesia in experimental models. Phytoconstituents in SV.CR such as oleanolic acid and caffeic acid might have played a significant neuroprotective role via modulation of oxidative stress and neurochemical aspects. Keywords GC-MS, HPTLC, Scopolamine-induced amnesia, anxiety, depression, Y-maze, escape latency, novel object recognition test Introduction Neurological disorders have been imposing a huge burden on people’s health globally. Unfortunately, this delinquency is claimed to grow exponentially in developing countries during the next decade. 1 The etiology of brain diseases may include congenital origin 2 or acquired at some stage of life due to some chemical imbalance, infection, trauma, cerebral and vascular disarrays. 3 Among numerous brain diseases, Alzhei- mer’s disease (AD), anxiety and depression are reported to predominantly affecting individuals and their families. 4 Alzheimer’s disease (AD) is a prevailing illness presenting memory loss in elder individuals that has affected 24 million populace worldwide. 5 The disease encompasses an initial decline in cognition that gradually influences all intellectual functions resulting in an individual’s dependency on others for basic daily activities. 6 It involves progressive neurodegeneration resulting in 1 Department of Pharmacology, Faculty of Pharmacy, Bahauddin Zakariya University, Multan, Pakistan 2 Department of Pharmacy, The Women University, Multan, Pakistan 3 Department of Pharmacy Practice, Faculty of Pharmacy, Bahauddin Zakariya University, Multan, Pakistan 4 Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia 5 Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia Received 03 February 2021; received revised 03 February 2021; accepted 05 February 2021 Corresponding Authors: Imran Imran, Department of Pharmacology, Faculty of Pharmacy, Bahauddin Zakariya University 60800, Multan, Pakistan. Email: imran.ch@bzu.edu.pk Faleh Alqahtani, Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia. Email: afaleh@ksu.edu.sa Dose-Response: An International Journal January-March 2021:1-18 ª The Author(s) 2021 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/1559325821998486 journals.sagepub.com/home/dos Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).