Anti-inflammatory effect of quinoline alkaloid skimmianine isolated from Ruta graveolens L.
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Inflammation Research
ORIGINAL RESEARCH PAPER
Anti-inflammatory effect of quinoline alkaloid skimmianine isolated from Ruta graveolens L. M. Ratheesh • G. Sindhu • Antony Helen
Received: 1 February 2012 / Revised: 25 November 2012 / Accepted: 2 January 2013 / Published online: 24 January 2013 Ó Springer Basel 2013
Abstract Objective The present study evaluates the anti-inflammatory effect of the quinoline alkaloid skimmianine (SKM), isolated from Ruta graveolens L., against carrageenan-induced acute inflammation. Methods SKM at a dose of 5.0 mg/kg body weight was found to be the minimal concentration for maximal edema inhibition. Carrageenan suspension was administered into the sub-plantar tissue of the right hind paw 1 h after SKM and diclofenac (20 mg/kg) administration (i.p.). Paw edema was determined 3 h after carrageenan administration. The rats were then killed and mRNA expressions of TNF-a and IL-6, levels of PGE2 and TBARS, activities of COX-2, 5-LOX, SOD, catalase, glutathione peroxidase (GPx) and myeloperoxidase (MPO) and the level of nitrite were measured. Results SKM treatment resulted in a decrease in the mRNA levels of TNF-a and IL-6, which are upstream events of the inflammatory cascade. The levels of PGE2 and NO and the activities of COX-2 and 5-LOX were also significantly reduced after SKM treatment. Neutrophil infiltration, lipid peroxidation and associated oxidative stress in the paw tissue were reduced following SKM treatment. Conclusion These results support the anti-inflammatory properties of skimmianine and its multi-targeted mechanism of action, suggesting its potential therapeutic efficacy in various inflammatory diseases.
Responsible Editor: Jerauld Skotnicki. M. Ratheesh G. Sindhu A. Helen (&) Department of Biochemistry, Kerala University, Trivandrum, India e-mail: [email protected]
Keywords In-vivo inflammation Inflammatory models Inflammation Oxidative stress
Introduction Inflammation is essentially a defensive response aimed at protecting organisms against physical, chemical and infective insults. Frequently, however, dysregulation of this response leads to damage of normal tissues. Prostaglandin E2 (PGE2), a key mediator of inflammatory response, is generated at sites of inflammation in substantial amounts from arachidonic acid by the enzyme cyclooxygenase (COX) and mediates many of the associated pathological features [1]. One of the early cellular events in inflammation is the infiltration/localization of polymorphonuclear leukocytes (PMN). The enzyme myeloperoxidase (MPO), present in the azurophilic granules of PMN, is unique to neutrophils and monocytes/macrophages. However, monocytes contain only one third of the MPO found in PMN’s. MPO activity can be used as an indicator of neutrophil accumulation [2]. Nitric oxide (NO) plays an important role in inflammation and inhibitors of NO synthase (NOS) have been shown to reverse several classic inflammatory symptoms [3]. The pro-inflammatory cytokine, tumor necrosis factor-a (TNF-a) was observed to stimulate neutro
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