Table of Contents
ISRN Pharmacology
Volume 2012, Article ID 479570, 8 pages
Research Article

Hesperidin Ameliorates Immobilization-Stress-Induced Behavioral and Biochemical Alterations and Mitochondrial Dysfunction in Mice by Modulating Nitrergic Pathway

1Department of Pharmacology, PES College of Pharmacy, Bangalore 560050, India
2Biomedical Research Centre, Sheffield Hallam University, Sheffield S11 OW, UK
3Department of Pharmacology, Al-Ameen College of Pharmacy, Bangalore 560027, India
4Department of Biochemistry, Jayadeva Institute of Cardiovascular Sciences and Research, Bangalore 560069, India

Received 12 November 2011; Accepted 20 December 2011

Academic Editors: V. C. Abilio and S. Tsuruoka

Copyright © 2012 G. L. Viswanatha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The present study was aimed to evaluate the protective effect of hesperidin against immobilization-stress-induced alterations in biochemical, behavioral, and mitochondrial functions in mice. In many instances neuroscientists have reported that acute immobilization stress for 6 h resulted in anxiety and impaired locomotor activity due to excess oxidative-nitrergic stress, depletion of antioxidant defense mechanisms, and mitochondrial dysfunction in animals. In the present study, 6 h of acute immobilization stress had significantly altered the behavioral (anxiety and memory) and biochemical parameters coupled with mitochondrial dysfunction in Swiss albino mice. Fourteen days of pretreatment with Hesperidin (50 and 100 mg/kg, p.o.) significantly and dose-dependently inhibited the behavioral and biochemical alterations and mitochondrial dysfunction caused by acute immobilization stress. Furthermore, pre-treatment of L-arginine (50 mg/kg, i.p.), a nitric oxide precursor, reversed the protective effect of Hesperidin (50 and 100 mg/kg) ( 𝑃 < 0 . 0 5 ). In contrast, pretreatment of L-NAME (5 mg/kg, i.p.), a nitric oxide synthase inhibitor, potentiated the protective effect of Hesperidin ( 𝑃 < 0 . 0 5 ). These results suggest the possible involvement of nitrergic pathway in the protective effect Hesperidin against immobilization-stress-induced behavioral, biochemical, and mitochondrial dysfunction in mice.