Users Online: 1094

Home Print this page Email this page Small font sizeDefault font sizeIncrease font size

Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 
     
ORIGINAL ARTICLE
Year : 2014  |  Volume : 4  |  Issue : 3  |  Page : 131-138

Effect of Ashwagandha (Withania somnifera) against chronic constriction injury induced behavioral and biochemical alterations: Possible involvement of nitric oxide mechanism


Department of Pharmacology, Neuropharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre for Advance Studies, Punjab University, Chandigarh, India

Correspondence Address:
Anil Kumar
Neuropharmacology Division, Department of Pharmacology, University Institute of Pharmaceutical Sciences, UGC Centre for Advance Studies, Punjab University, Chandigarh 160 014
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.132664

Rights and Permissions

Aim: Neuropathic pain (NP) arises due to lesion or disease in somatosensory nervous system. Recent reports indicate the role of Withania somnifera (WS) in various inflammatory pain conditions. The objective of the present study was to explore the possible protective effect of WS against chronic constriction injury (CCI) induced NP in rats. Materials and Methods: CCI of sciatic nerve was performed in male Wistar rats. Various behavioral parameters (thermal hyperalgesia, cold allodynia) followed by biochemical parameters (lipid peroxidation, reduced glutathione, catalase and nitrite) were assessed in sciatic nerves. Drugs were administered consecutively for 21 days from the day of surgery. CCI to sciatic nerve significantly caused thermal hyperalgesia, cold allodynia and oxidative damage in the sciatic nerves when compared with naive and sham control. Results: Chronic administration of WS (100 and 200 mg/kg, p.o.) significantly attenuated hyperalgesia, cold allodynia and oxidative damage (as indicated by reduction in lipid peroxidation, nitrite concentration, restoration of reduced glutathione and catalase activity). Further, L-NAME (5 mg/kg, i.p.) pre-treatment with WS (100 mg/kg, p.o.) significantly potentiated the protective effect of WS which was significant when compared with their effect per se However, L-arginine (100 mg/kg, i.p.) pre-treatment with WS (100 mg/kg, p.o.) significantly reversed the protective effects of WS in sciatic nerve. Conclusion: Result of present study suggests that nitric oxide mechanism could be involved in the protective effect of WS against CCI induced behavior alterations and oxidative damage in rats.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed3296    
    Printed59    
    Emailed0    
    PDF Downloaded223    
    Comments [Add]    
    Cited by others 3    

Recommend this journal