Pharmacological and biochemical modulation of stress markers by L-NAME and L-Ascorbic acid in chronic restraint model in Wistar rats

Authors

  • Giridhari Pal Research Scholar, Department of Pharmacology, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi-110007
  • Vishwajeet Rohil Assistant Professor, Department of Biochemistry, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi-110007 http://orcid.org/0000-0002-1400-0744
  • Razi Akhtar Medical Officer, Government of NCT, Delhi
  • Tapan Behl Senior Research Fellow, Department of Pharmacology, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi-110007, India
  • Sudha Bharati Scholar, Department of Material Science & Technology, IIT BHU, Varanasi
  • Trupti Rekha Swain Associate Professor, Department of Pharmacology, SCB Medical College, Utkal University, Odisha-753007
  • Mohammed Imran Associate Professor, Department of Medical Pharmacology, SHKMGM, Haryana-122107, India
  • Jyotirmoyee Jena Professor, Department of Pharmacology, VSS Medical College, Sambalpur University, Odisha-768017

DOI:

https://doi.org/10.3126/ajms.v8i1.16010

Keywords:

Restraint Stress, Chronic Stress, Antioxidant, N-nitro-L-arginine-methyl ester, L-Ascorbic acid

Abstract

Background: Stress is the psycho-physiologic reaction of the body to diverse stimuli including emotional or physical stimuli that imbalance the homeostasis and is also known to trigger various stress markers. Despite the stressors of different types, chronic stress in particular, is known to influence the physiological milieu and breakdown of adaptive mechanisms consequently aggravating the morbid states.  

Aims and Objectives: The present study was designed to evaluate the modulatory role of stress marker by N-nitro-L-arginine-methyl ester (L-NAME) and L-Ascorbic acid (L-AA) in experimental model of chronic restraint stress (RSx21) in Wistar rats.

Materials and Methods: MDA and GSH levels were determined by the method of Okhawa et al 1979 and Ellman 1959 respectively, the SOD and catalase levels were estimated by the method of Nandi and Chatterjee 1988 and Aebi 1984 respectively.

Results: Results from our study reveal the significant enhancement of malondialdehyde (MDA) level while significant attenuation of superoxide dismutase (SOD), reduced glutathione (GSH) and catalase levels in chronic stress group compared with vehicle (non-stress) group. The MDA level was found to be increased by L-NAME (10 and 50 mg/kg) in chronic restraint (RSx21) induced rats as compared to vehicle treated RS group. Antioxidant L-AA (100 and 200 mg/kg) significantly reduced MDA level in chronic stress situation. However, L-NAME and L-Ascorbic Acid were found to cause an increase in level of plasma SOD, GSH and catalase when compared with vehicle treated RS group. On the other hand, L-AA (100 and 200 mg/kg) reversed these RS induced changes in these oxidative parameters.

Conclusions: Hence, results from the study underlined the intricate role of antioxidants as evidenced by reversal of oxidative stress markers that command a vital role in the development of morbid condition.

Asian Journal of Medical Sciences Vol.8(1) 2017 15-20

Downloads

Download data is not yet available.
Abstract
780
PDF
786

Downloads

Additional Files

Published

2017-01-03

How to Cite

Pal, G., Rohil, V., Akhtar, R., Behl, T., Bharati, S., Swain, T. R., Imran, M., & Jena, J. (2017). Pharmacological and biochemical modulation of stress markers by L-NAME and L-Ascorbic acid in chronic restraint model in Wistar rats. Asian Journal of Medical Sciences, 8(1), 15–20. https://doi.org/10.3126/ajms.v8i1.16010

Issue

Vol. 8 No. 1 (2017)

Section

Original Articles

License

Authors who publish with this journal agree to the following terms:

  1. The journal holds copyright and publishes the work under a Creative Commons CC-BY-NC license that permits use, distribution and reprduction in any medium, provided the original work is properly cited and is not used for commercial purposes. The journal should be recognised as the original publisher of this work.
  2. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
  3. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).