Gastroprotective Activity of Violacein Isolated fromChromobacterium violaceumon Indomethacin-Induced Gastric Lesions in Rats: Investigation of Potential Mechanisms of Action

Author:

Antonisamy Paulrayer1,Kannan Ponnusamy2,Aravinthan Adithan1,Duraipandiyan Veeramuthu3,Valan Arasu Mariadhas3,Ignacimuthu Savarimuthu2,Abdullah Al-Dhabi Naif3,Kim Jong-Hoon1

Affiliation:

1. Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, 664-14 1GA, Duck Jin-Dong, Deokjin-gu, Jeonju City, Jeollabuk-do 561-756, Republic of Korea

2. Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai, Tamil Nadu 600 034, India

3. Department of Botany and Microbiology, Addiriyah Chair for Environmental Studies, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia

Abstract

Chromobacterium violaceum, Gram-negative bacteria species found in tropical regions of the world, produces a distinct deep violet-colored pigment called violacein. In the present study, we investigated whether violacein can promote a gastroprotective effect and verified the possible mechanisms involved in this action. For this study, an indomethacin-induced gastric ulcer rat model was used. The roles of biomolecules such as MPO, PGE2, pro- and anti-inflammatory cytokines, growth factors, caspase-3, NO, K+ATP channels, andα2-receptors were investigated. Violacein exhibited significant gastroprotective effect against indomethacin-induced lesions, while pretreatment with L-NAME and glibenclamide (but not with NEM or yohimbine) was able to reverse this action. Pretreatment with violacein also restored cNOS level to normal and led to attenuation of enhanced apoptosis and gastric microvascular permeability. Our results suggest that violacein provides a significant gastroprotective effect in an indomethacin-induced ulcer model through the maintenance of some vital protein molecules, and this effect appears to be mediated, at least in part, by endogenous prostaglandins, NOS, K+ATP channel opening, and inhibition of apoptosis and gastric microvascular permeability.

Funder

King Saud University

Publisher

Hindawi Limited

Subject

General Environmental Science,General Biochemistry, Genetics and Molecular Biology,General Medicine

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