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- Title
Hesperidin Ameliorates Immobilization-Stress-Induced Behavioral and Biochemical Alterations and Mitochondrial Dysfunction in Mice by Modulating Nitrergic Pathway.
- Authors
Viswanatha, G. L.; Shylaja, H.; Rao, K. S. Sandeep; Kumar, V. R. Santhosh; Jagadeesh, M.
- Abstract
The present study was aimed to evaluate the protective effect of hesperidin against immobilization-stress-induced alterations in biochemical, behavioral, and mitochondrial functions inmice. 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 dosedependently inhibited the behavioral and biochemical alterations and mitochondrial dysfunction caused by acute immobilization stress. Furthermore, pre-treatment of l-arginine (50mg/kg, i.p.), a nitric oxide precursor, reversed the protective effect of Hesperidin (50 and 100 mg/kg) (P < 0.05). In contrast, pretreatment of l-NAME (5mg/kg, i.p.), a nitric oxide synthase inhibitor, potentiated the protective effect of Hesperidin (P < 0.05). 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.
- Subjects
HESPERIDIN; IMMOBILIZATION stress; MITOCHONDRIAL membranes; OXIDATIVE stress; BIOCHEMICAL models; ARGININE; LABORATORY mice
- Publication
ISRN Pharmacology, 2012, p1
- ISSN
2090-5165
- Publication type
Article
- DOI
10.5402/2012/479570