Drug Res (Stuttg) 2017; 67(07): 425-431
DOI: 10.1055/s-0043-108552
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Ellagic Acid Administration Negated the Development of Streptozotocin-Induced Memory Deficit in Rats

Nitin Bansal
1   Department of Pharmacology, ASBASJSM College of Pharmacy, Bela, Ropar, India
,
Pushplata Yadav
1   Department of Pharmacology, ASBASJSM College of Pharmacy, Bela, Ropar, India
,
Manish Kumar
1   Department of Pharmacology, ASBASJSM College of Pharmacy, Bela, Ropar, India
› Author Affiliations
Further Information

Publication History

received 10 August 2016

accepted 01 April 2017

Publication Date:
12 May 2017 (online)

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Abstract

Rampant production of pro-oxidants and inadequate antioxidant availability in brain exert oxidative stress, which in synergism with impaired glucose metabolism and inflammation leads to neurodegeneration and cognitive deficits. Ellagic acid (EGA) is a phenolic compound present in various fruits and is reported to possess robust antioxidant and anti-inflammatory properties. The present study investigated the effect of EGA administration on streptozotocin (STZ) induced dementia in rats. Bilateral intracerebroventricle (ICV) injection of STZ (3 mg/kg) was given to Wistar rats (200 g) on day 1 and 3. EGA (17.5 and 35 mg/kg) was administered orally to rats for 28 days daily. The spatial memory of rats was quantified by using Morris water maze and elevated plus maze. Brain TBARS, GSH and TNF-α were also measured. Administration of EGA prevented the induction of STZ-ICV 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 retrieval trial in Morris water maze test, and reduction (p<0.05) in transfer latency in elevated plus maze test. Furthermore, both the doses of EGA attenuated STZ-ICV induced rise in brain TBARS as well as TNF-α and simultaneously enhanced the GSH content. Thus, EGA ameliorated STZ-induced dementia by probably restoring the balance between cellular pro-oxidants and anti-oxidants in brain of rats.