Browsing by Author "Nitin Bansal"

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    Anxiolytic activity of Angiotensin-Receptor-Blocker in Experimental Models of Anxiety in Mice
    (Chitkara University Publications, 2014-11-30) Syed Rehan Hasan; Manish Sinha; Nitin Bansal
    The present study aimed to explore the role of Angiotensin- Receptor-Blocker in the management of anxiety. Male Swiss albino mice of age 6-8 weeks and weight 25-30 g were used in the present study. Candesartan (Angiotensin receptor blocker) was administered in two doses (1 and 2 mg/kg; i.p.) to mice for 14 successive days regularly. Anxiety was induced in mice by two different methods: (i) exposing the mice to immobilization stress for a period of 6 h daily for 7 consecutive days; (ii) administration of caffeine (25 mg/kg; i.p.) daily for 7 days. Elevated Zero Maze and Open Field Apparatus were used to evaluate the level of anxiety in different groups. After behavioral evaluation, the animals were sacrificed and their brains were used for estimation TBARS, GSH and Nitrite levels in the brain. Administration of Candesartan (1 and 2 mg/kg; i.p) for 14 successive days significantly (p<0.05) reduced anxiety due to immobilization stress and caffeine induced anxiety. Candesartan (1and 2 mg/kg; i.p) treated mice showed an increase (p<0.05) in GSH levels while a decrease (p<0.05) in TBARS and nitrite levels in brain. Thus, candesartan may prove to be a useful remedy for the management of anxiety owing to its neuroprotective and antioxidant activity.
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    Dementia: An Overview
    (Chitkara University Publications, 2014-05) Nitin Bansal; Milind Parle
    Dementia is a neurodegenerative disorder characterized by progressive and continuous loss of cognitive functions. The neuropsychiatric symptoms include apathy; agitation and depression. As the disorder progresses, the patient gradually becomes dependent on others to perform routine daily activities. Various underlying diseases or disorders are the root cause of the syndrome of dementia. Each of these disorder or disease is characterized by a specific signs and symptoms in combination with a presumed underlying neuropathology. Alzheimer’s disease is the most prevalent cause of dementia. The second most prevalent cause is vascular dementia. In this review, the clinical types, pathophysiology and pharmacotherapy is summarized.
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    Ellagic Acid Administration Reverses Colchicine- Induced Dementia in Rats
    (Chitkara University Publications, 2016-05-07) Jaspreet Kaur; Manish Kumar; Nitin Bansal
    The late-onset sporadic type of Alzheimer’s disease is characterised by chronic oxidative stress, neuroinflammation and cognitive dysfunction. Ellagic acid is a naturally occurring polyphenol known to possess robust antioxidant property. In the present study, memory enhancing potential of ellagic acid has been explored against ICV colchicine induced dementia in rats. Colchicine (15μg/rat) was administered to Wistar rats (200g) through intracerebroventricular (ICV) route by using stereotaxic apparatus. ICV colchicine induces Alzheimer’s disease like changes in the brain such as rampant free radical production, neuroinflammation and selective neurodegeneration in hippocampus and cortex by acting as an antitubulin agent (mitotic poison). Ellagic acid (17.5 and 35 mg/kg, p.o.) was administered to rats for 25 successive days. Morris water maze and elevated plus maze paradigms were utilized to assess the spatial memory of rats. Oxidative stress biomarkers along with TNF-α were also measured in brain of rats. Ellagic acid prevented the ICV colchicine triggered cognitive deficits as evident by a significant (p<0.05) reduction in mean escape latency during acquisition trial and increased (p<0.05) time spent in target quadrant during probe trial in Morris water maze test, and reduction (p<0.05) in transfer latency in elevated plus maze test. Furthermore, both the doses of ellagic acid attenuated ICV colchicine induced rise in brain TBARS as well as TNF-α and simultaneously enhanced the GSH content.Ellagic acid prevented the brain of rodents from dementing effects of colchicine by attenuating the oxidative damage.