Arachidonic acid induced edema

P. lanceolata Wound Anti-inflammatory -lnhibit]on of arachidonic acid-induced edema [61]... 

Hall, E.D. and Travis, M.A. (1988) Inhibition of arachidonic acid-induced vasogenic brain edema by the non-glucocorticoid 21-aminosteroid U74006F, Brain Res. 451, 350-352. 

Plantamajoside (30) from P. asiatica and acteoside from P. lanceolata were tested for inhibitory effect on arachidonic acid-induced mouse ear edema [49]. Plantamajoside (30) showed a high inhibitory effect with inhibitions of 12 % at 1 mg / ear and of 25 % at 3 mg / ear. On the other hand, acteoside (1) showed a weak inhibitory effect with inhibitions of 6 % at 1 mg / ear and of 14 % at 3 mg / ear. This result showed good correlation with the inhibition of cyclic AMP phosphodiesterase and 5-lipoxygenase. 

Murai M, Tamayama Y, Nishibe S (1995) Phenylethanoids in the herb of Plantago lanceolata and inhibitory effect on arachidonic acid-induced mouse ear edema. Planta Med 61(5) 479-480 Muravyova DA (1978) Farmakognoziya (Pharmacognosy). Meditsina, Moscow (in Russian)... 

These steioids aie capable of preventing or suppressing the development of the sweUing, redness, local heat, and tenderness which characterize inflammation. They inhibit not only the acute symptoms of the inflammatory process, such as edema, fibrin deposition, and capillary dilatation, but also the chronic manifestations. There is evidence that glucocorticoids induce the synthesis of a protein that inhibits phosphoHpase A 2 (60), diminishing the release of arachidonic acid from phosphoHpids (Fig. 2), thereby reducing chemotaxis and inflammation. 

Assaad, A., Trotz, M., Moore, D., Nold, J, Corcoran, K., Hurt, H., Keeler, J., Phillips, K., and Said, S.I. 1990. Arachidonic acid metabolites as early markers of phosgene-induced acute lung injury and pulmonary edema. World Conference on Lung Health. Boston, MA. May 20-24. Am. Rev. Respir. Dis. 141 A420. 

It has been shown that arachidonic acid metabolism could contribute to the pathogenesis of cerebral edema. Treatment with indomethacin, a COX inhibitor, nordihydroguaiaretic acid, a LOX inhibitor, or their combination significantly reduced vasogenic edema induced by freezing lesions (Yen and Lee, 1987). 

It was observed that rats with a transient MCA occlusion have a larger brain infarction when recombinant human IL-1 P is injected into the lateral ventricle immediately after reperfusion [7,41]. Similar results have been obtained in rats with a permanent MCA occlusion [7,42]. The intraventricular injection of recombinant human IL-1 p also enhances the formation of brain edema and increases both the number of neutrophils in ischemic areas and neutrophil-endothelial cell adhesion. The most widely recognized functions of IL-1 appear to be the induction of endothelial cell adhesion molecule expression and the promotion of neutrophil tissue infiltration [7,41]. These observations suggest that IL-1 may play a deleterious role in cerebral ischemia. Studies showing a reduction in infarct size after the administration of IL-1 antagonists or inhibitors provide further evidence of the importance of IL-1 in cerebral ischemia [41,43-49]. The possible harmful mechanisms induced or activated by IL-1 include fever, increased heart rate and arterial blood pressure, enhancement of N-methyl-D-aspartate-mediated injury, proliferation of microglia, release of arachidonic acid, and stimulation of NO synthesis [7,50]. 

Finally, routine animal models for inflammatory diseases can be used for testing the in vivo efficacy of selectin antagonists the murine peritonitis model and the ear edema model are the most common. In the murine peritonitis model [200], the migration of leukocytes in response to an acute inflammatory stimulus is assessed by intraperitoneal injection of thioglycolate. In the arachidonic acid- or croton oil-induced ear edema model [131,201], inflammation is measured as neutrophil infiltration, represented by myeloperoxidase activity in ear biopsy samples. 

Inflammation is a normal and complex reaction by the body to an injury. Aloe has been used in traditional medicine for its anti-inflaimnatoiy use. The aqueous and chloroform extracts of aloe inhibit the effect on carrageen induced edema. This effect was associated with an inhibitory action on the arachidonic acid pathway via cyclooxygenase 68). Aloe gel components were able to suppress bacterial induced pro-inflarmnatoiy production of cytokines (systematically elevated after a bacterial invasion), namely TNF-a and IL-p 69). 

Capsaicin is a natural compound that has been described as both anti-genotoxic and anti-carcinogenic. In addition, it is surmised to have a potential chemopreventive activity [119]. The compound s antiinflammatory properties have been demonstrated in different in vivo pharmacological tests, which have shown that it inhibits, among others, carrageenan-induced inflammation in rats and croton oil-induced mouse ear edema. These effects are associated with its interference of phospholipase A2 (PLA2), the enzyme that produces arachidonic acid from the membrane phospholipids. Moreover, the proapoptotic effects of capsaicin are widely documented in the literature [120]. 

Triterpenes are widely distributed in plants, and in many cases are the principles responsible for their anti-inflammatory effects. Many of these compounds are active in different in vivo experimental models such as hind paw edema induced by carrageenan, serotonin and phospholipase A2 ear edema induced by phorbol and daphnane esters, ethylphenylpropiolate, arachidonic acid and capsaicin adjuvant arthritis and experimental models of allergy. Other effects have been studied in vitro, and some triterpenes are active against inflammatory enzymes like 5-lipoxygenase, elastase and phospholipase A2. Others inhibit histamine, collagenase and interleukin release, lipid peroxidation and free radical-mediated processes, metabolism of endogenous corticoids, and complement and protein-kinase activities. 

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