s-5682 has been researched along with Inflammation* in 3 studies
1 review(s) available for s-5682 and Inflammation
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Cellular basis of inflammation, edema and the activity of Daflon 500 mg.
Inflammation activates leukocytes causing the release of agents that disrupt the endothelial barrier to such an extent that retention of plasma protein is impaired. This phenomenon can be observed using microvascular methods in which ischemia-reperfusion-induced inflammation-like condition are analyzed in terms of the increased adherence of leukocytes to the venular endothelium. Pretreatment with Daflon 500 mg, a purified, micronized, flavonoid fraction consisting of 90% diosmin and 10% hesperidin, prior to the induction of 4 h of tourniquet ischemia significantly lowers the number of adherent leukocytes. This observation is linked to the protective effect of flavonoids in the treatment of edema, as decreased activation is also associated with a decreased platelet and complement system activation, leading to a lowered release of histamine and decreased leukocyte-dependent endothelial damage. It is proposed that attenuation of leukocyte adherence during ischemia-reperfusion is evidence of the protective endothelial effect of Daflon 500 mg and its ability to control edema in clinical situation. Topics: Animals; Diosmin; Drug Combinations; Edema; Flavonoids; Hesperidin; Inflammation; Leukocytes; Microcirculation; Reperfusion Injury; Skin | 1995 |
2 other study(ies) available for s-5682 and Inflammation
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Pharmacologic properties of Daflon 500 mg.
Some pharmacologic activities of a micronized flavonoid complex consisting of 90% diosmin + 10% hesperidin (Daflon 500 mg*) have been investigated by use of various experimental models: (1) interference with mechanisms of edema (synthesis of arachidonic acid derivatives, microvascular hyperpermeability induced by bradykinin, ischemia, or streptozotocin), (2) interference with lymphatic drainage (thoracic duct fistula in the dog).. Daflon 500 mg inhibited prostaglandin E2 (PGE2) and thromboxane A2 (TxA2) synthesis during a one-month oral daily treatment (100 mg.kg-1.day-1) in the rat, after induction of chronic inflammation by subcutaneous implantation of sponge fragments. Microvascular hyperpermeability induced by bradykinin or ischemia in the rat cremaster muscle was reduced after an oral treatment with Daflon 500 mg (100 mg.kg-1 twice daily). Microvascular hyperpermeability of the streptozotocin-induced diabetic rat was antagonized when Daflon 500 mg (300 mg.kg-1 once daily) was given orally as a preventive treatment. In the anesthetized dog, an increase in lymphatic flow, correlated with administered doses, was observed after IV injection of Daflon 500 mg. Lymphatic flow was maximal twenty minutes after injection of the drug (12.5 mg.kg-1) and was three times higher than the basal flow.. The protective effect of Daflon 500 mg against the formation of perivascular edema and its therapeutic value in the treatment of venous stasis could be explained by its inhibitory activity on the inflammatory process or ischemia-induced hyperpermeability and by its stimulatory effect on the pulsatile activity of lymphatic vessels. Topics: Animals; Capillary Permeability; Diabetes Mellitus, Experimental; Dinoprostone; Diosmin; Dogs; Drug Combinations; Edema; Flavonoids; Hesperidin; Inflammation; Kidney Glomerulus; Lymph; Muscles; Rats; Thoracic Duct; Thromboxane B2 | 1994 |
Mediators involved in inflammation: effects of Daflon 500 mg on their release.
Each step of an inflammatory reaction is triggered by one or several chemical or biological mediators such as arachidonic acid derivatives (prostaglandins [PG], leukotrienes [LT], or thromboxanes [TX]), vasoactive amines (histamine or serotonin), and oxygen free radicals (superoxide ion, O2-, or hydrogen peroxide, H2O2). In perivenous inflammation, these mediators play a prominent role in favoring vasodilatation (histamine), increasing membrane permeability (PGE2, histamine, free radicals) and providing a chemotactic signal for specialized cells, ie, neutrophil polynuclears, macrophages, lymphocytes (LTB4, free radicals). The antiinflammatory effects of Daflon 500 mg,* a micronized purified flavonoid fraction (90% diosmin, 10% hesperidin), were studied in different in vivo and in vitro models. In a model of inflammatory granuloma in the rat, Daflon 500 mg (100 mg/kg, orally) reduced edema formation and inhibited the synthesis for PGE2 (78.5%), PGF2 alpha (45.2%) and TXB2 (59.5%) (Damon et al, Arzneim-Forsch/Drug Res 37:1149-1153, 1987). Intravenous injection of Daflon 500 mg (25 and 50 mg/kg) reduced the hyperglycemia induced by injection of alloxan in rat. This effect of Daflon 500 mg was linked to its ability to scavenge active oxygen radicals, demonstrated in vitro using human neutrophils (Lonchampt et al, Arzneim-forsch/Drug Res 39:882-885, 1989) or mouse peritoneal macrophages (Bodinier et al, manuscript in preparation) stimulated by zymosan. The free radical scavenger effect of Daflon 500 mg is observed at concentrations ranging from 10(-7) M to 10(-4) M, with half-maximal effect between 10(-6) M and 10(-5) M. Thus, Daflon 500 mg behaves as a potent protective agent against inflammatory disorders. These properties may explain, at least in part, the clinical activity of Daflon 500 mg and justify its therapeutic use. Topics: Alloxan; Animals; Anti-Inflammatory Agents; Blood Glucose; Diabetes Mellitus, Experimental; Diosmin; Drug Combinations; Flavonoids; Free Radicals; Granuloma; Hesperidin; Humans; Inflammation; Kidney Glomerulus; Macrophages; Mice; Neutrophils; Permeability; Prostaglandins; Rats; Thromboxane B2 | 1994 |