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      Anti-inflammatory and membrane stabilizing properties of methyl jasmonate in rats

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          The present investigation was carried out to evaluate anti-inflammatory and membrane stabilizing properties of methyl jasmonate (MJ) in experimental rat models of acute and chronic inflammation. The effects of MJ on acute inflammation were assessed using carrageenan-induced rat’s paw edema model. The granuloma air pouch model was employed to evaluate the effects of MJ on chronic inflammation produced by carrageenan in rats. The number of white blood cells (WBC) in pouch exudates was estimated using light microscopy. The levels of biomarkers of oxidative stress, such as malondialdehyde (MDA), glutathione (GSH) and activity of antioxidant enzymes in the exudates, were determined using spectrophotometry. The membrane stabilizing property of MJ was assessed based on inhibition of hemolysis of rat red blood cells (RBC) exposed to hypotonic medium. Our results indicated that MJ (25–100 mg·kg −1, i.p.) produced significant anti-inflammatory activity in carrageenan-induced paw edema in rats ( P < 0.05). MJ reduced the volume of pouch exudates and the number of WBC in carrageenan-induced granulomatous inflammation. It also exhibited potent antioxidant and membrane stabilizing activities. In conclusion, these findings suggest the therapeutic potentials of methyl jasmonate in disease conditions associated with inflammation and its anti-inflammatory activity may be related to its antioxidant and membrane stabilizing activities.

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          Most cited references 13

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          Levels of glutathione, glutathione reductase and glutathione S-transferase activities in rat lung and liver

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            Prospects for the use of antioxidant therapies.

            Free radical oxidative stress has been implicated in the pathogenesis of a variety of human diseases. Natural antioxidant defences have been found to be defective in many of the same diseases. This has led to suggestions that oxidative damage and therefore disease progression may be retarded by supplementing natural antioxidant defences. Potential antioxidant therapy includes natural antioxidant enzymes and vitamins or synthetic agents with antioxidant activity. Diseases where antioxidant therapy may be beneficial include diabetes mellitus, reperfusion injury, inflammatory diseases and the prevention of chronic processes such as atherosclerosis and carcinogenesis. Further well controlled prospective clinical trials of antioxidants are required to establish the efficacy and tolerability of antioxidant therapy in the treatment of human diseases.
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              Inflammation and the mechanism of action of anti-inflammatory drugs.

               J R Vane,  R Botting (1987)
              Inflammation is caused by release of chemicals from tissues and migrating cells. Most strongly implicated are the prostaglandins (PGs), leukotrienes (LTs), histamine, bradykinin, and, more recently, platelet-activating factor (PAF) and interleukin-1. Evidence for their involvement comes from studies with competitive antagonists for their receptors and inhibitors of their synthesis. H1 histamine antagonists are effective for hay fever and some skin allergies such as urticaria, which indicates the importance of histamine in these conditions. Symptoms of rheumatoid arthritis are alleviated by the aspirinlike anti-inflammatory drugs, which inhibit the cyclo-oxygenase enzyme and reduce synthesis of prostanoids. Corticosteroids prevent the formation of both PGs and LTs by causing the release of lipocortin, which by inhibition of phospholipase A2 reduces arachidonic acid release. They suppress the inflammation of rheumatoid arthritis and asthma. Currently, high doses of nonsedating H1 antihistamines and PAF antagonists are being tested for the treatment of allergic asthma.

                Author and article information

                Chinese Journal of Natural Medicines
                20 March 2017
                : 15
                : 3
                : 202-209
                1Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences University of Ibadan, Ibadan, Nigeria
                2Department of Pharmacology, Faculty of Basic Medical Sciences, Olabisi Onabanjo University, Ago-Iwoye, Nigeria
                3Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
                Author notes
                *Corresponding author: UMUKORO Solomon, Tel: 234-813-0897439, Fax: 234-241-3546, E-mail: umusolo@

                These authors have no conflict of interest to declare.

                Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.


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