Effect of rifampicin, isoniazid on acute and subacute inflammation in male Wistar rats: an experimental study

Priya Gandigawad; Anil P. Hogade; P. A. Patil; P. R. Malur

doi:10.18203/2319-2003.ijbcp20150372

Authors

Priya Gandigawad Department of Pharmacology, SDM College of Medical Sciences, Dharwad, Karnataka, India
Anil P. Hogade Department of Pharmacology, J. N. Medical College, Belgaum, Karnataka, India
P. A. Patil Department of Pharmacology, J. N. Medical College, Belgaum, Karnataka, India
P. R. Malur Department of Pathology, J. N. Medical College, Belgaum, Karnataka, India

DOI:

https://doi.org/10.18203/2319-2003.ijbcp20150372

Keywords:

Rifampicin, Isoniazid, Aspirin, Inflammation

Abstract

Background: Tuberculosis (TB) is characterized by significant inflammation leading to complications like pulmonary fibrosis, constrictive pericarditis, etc. Drugs possessing anti-inflammatory activity can reduce the complications of infections occurring due to inflammation and fibrosis. To study the effect of rifampicin, isoniazid on acute and subacute models of inflammation in male Wistar rats.

Methods: The in vivo anti-inflammatory activity of rifampicin, isoniazid was studied using acute (carrageenan paw edema) and sub-acute (cotton pellet granuloma and histopathologic examination of grass pith) models of inflammation.

Results: Rifampicin and isoniazid used in the present study showed significant anti-inflammatory activity in acute as well as subacute models of inflammation.

Conclusion: Rifampicin and isoniazid when administered to treat TB can reduce complications of TB by virtue of its anti-inflammatory activity.

Metrics

Metrics Loading ...

References

Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Diseases. 8th Edition. Philadelphia: Elsevier Publishers; 2010.

Park K. Park’s Textbook of Preventive and Social Medicine. 18th Edition. Jabalpur: M/s Banarasidas Bhanot Publishers; 2005.

Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al. Harrison’s Principles of Internal Medicine. 17th Edition. New York: McGraw Hill Publishers; 2008.

Brunton LL, Lazo JS, Parker KL. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 12th Edition. New York: McGraw Hill Publishers; 2011.

Pahlevan AA, Wright DJ, Bradley L, Smith C, Foxwell BM. Potential of rifamides to inhibit TNF-induced NF-kappaB activation. J Antimicrob Chemother. 2002;49(3):531 4.

dos Santos Fde J, Ximenes VF, da Fonseca LM, de Faria Oliveira OM, Brunetti IL. Horseradish peroxidase-catalyzed oxidation of rifampicin: reaction rate enhancement by co-oxidation with anti-inflammatory drugs. Biol Pharm Bull. 2005;28(10):1822-6.

Yuhas Y, Azoulay-Alfaguter I, Berent E, Ashkenazi S. Rifampin inhibits prostaglandin E2 production and arachidonic acid release in human alveolar epithelial cells. Antimicrob Agents Chemother. 2007;51(12):4225-30.

Mlambo G, Sigola LB. Rifampicin and dexamethasone have similar effects on macrophage phagocytosis of zymosan, but differ in their effects on nitrate and TNF-α production. Int Immunopharmacol. 2003;3(4):513-22.

Kucharz EJ, Sierakowski SJ. Studies on immunomodulatory properties of isoniazid: v. Influence of isoniazid on secretion of interleukin-1. J Hyg Epidemiol Microbiol Immunol. 1992;36(1):119-22.

Tentori L, Graziani G, Porcelli SA, Sugita M, Brenner MB, Madaio R, et al. Rifampin increases cytokine-induced expression of the CD1b molecule in human peripheral blood monocytes. Antimicrob Agents Chemother. 1998;42(3):550 4.

Yuhas Y, Berent E, Ovadiah H, Azoulay I, Ashkenazi S. Rifampin augments cytokine-induced nitric oxide production in human alveolar epithelial cells. Antimicrob Agents Chemother. 2006;50(1):396-8.

Turner RA. Screening Methods in Pharmacology. New York and London: Academic Press Inc.; 1965.