Carrageenan Edema In Rats Research Articles

Experimental study of anti-inflammatory properties of exposure “Venosten”

Topicality. The presence of inflammatory process in diseases of veins caused the study of anti-inflammatory activity of the dense extract “Venosten”, which was investigated on models of inflammation with various mechanisms of development: carragenin and zimozanovyh edema. The aim of this work was to study the anti-inflammatory properties of the new dense “Venosten” extract in the dose range and establish an effective dose for this type of pharmacological activity. Materials and methods. At the first stage of the study, the study of anti-inflammatory properties on the model of carrageenan edema in rats. It is known that in the pathogenesis of carrageenitis inflammation in 1.5-5.5 hours after the introduction of flogogenic GHG plays a leading role, this allows us to conclude about the effect of the investigated extract on the cyclooxygenase system. In order to establish the ability of the thick extract of “Venosten” to suppress the activity of the key enzymes of the transformation of arachidonic acid in the next stage, we used a model of zymosan edema, whose mechanism of development is the formation of LT (0.5 hours). The anti-inflammatory activity of the thick extract “Venosten” was studied in doses 25 mg/kg, 50 mg/kg and 100 mg/kg. Results and discussion. The essential extract of “Venosten” in a dose of 100 mg/kg reduced the new caraphaea by a new swelling by 3 hours in 1.8 times (anti-eczual activity 42.2 %). Pre-administration of the “Venosten” Extract of 100 mg/kg significantly impairs the development of zymosan edema. Thus, 0.5 hours after the administration of zymosan to animals, in the rat treated with the “Venosten” extract, the edema was significantly lower than 1.5 times in the control group of pathology. The anti-exudative activity was 32.6 %. Conclusions. Extract “Venosten” in a dose of 100 mg/kg showed a pronounced anti-exudative activity and the ability to suppress the synthesis of prostaglandins and moderately affect the synthesis of leukotrienes.

Potentiative effect of angiotensin converting enzyme inhibitor on carrageenan edema in rats and the role of tissue kininogen.

Roles of kininogens in the development of potentiation of carrageenan edema in rats by angiotensin converting enzyme (ACE, = kininase II) inhibitor were studied. Carrageenan-induced edema was potentiated by oral administration of YS980, an ACE inhibitor, at a dose of 1 mg/kg 0.5 h before carrageenan injection. Intravenous injection of bromelain, a kininogen (KGN) depletor, at 3 mg/kg produced reduction of plasma KGN (total and high molecular weight KGN), which resulted in suppression of carrageenan edema and suppression of edema potentiation induced by YS980. Even after the plasma KGN level and inflammatory response to carrageenan returned to normal 24 h after the administration of bromelain, the potentiative effect of YS980 on the carrageenan edema remained suppressed. Thus, some factor other than plasma KGN is thought to be involved in the potentiation mechanisms on the carrageenan edema by YS980. Partially purified KGN from rat plasma (0.1 mg/site: liberated 4.4 X 10(-8) g bradykinin eq by trypsin digestion) completely restored the suppressed potentiation to normal by local preinjection to the inflamed site. In addition, such restoration was not observed in the animal in which plasma KGN was reduced 3 h after administration of bromelain. These results suggest that KGN, not only in plasma but also in tissue, play an active role in the development of potentiation of carrageenan edema by ACE inhibitor.

Potentiative effect of ACE inhibitor on carrageenan edema in rats (VI) : Involvement of kininogens in the development of potentiation.

We already reported that angiotensin converting enzyme (ACE) inhibitor YS980 potentiated the carrageenan (Carr) edema in the rat hind paw via an inhibition of kininase II (=ACE) in the inflamed sitel) and that the potentiative activity of YS980 reflected the plasma kininogen level2). In the present study, the role of tissue kininogen was examined in the development of potentiative effect of YS980 on Carr edema. RESULTS: Carr edema was produced in the right or left hind paw of each animal 24 hr after the injection of bromelain (0.1 mg/right paw) which was thought to deplete the local kininogen in the injection site. Potentiation of Carr edema by YS980 did not develop in the bromelain-treated side (right paw), but it developed in the opposite site. Partially purified kininogen from rat plasma (0.1 mg/paw: this amount of the protein was thought to release 10−8 g bradykinin by trypsin treatment) restored the suppressed potentiation in the bromelain-treated paw, but such restoration was not observed in the rat of which plasma kininogen level was reduced by i.v. injection of bromelain. In conclusion, it is suggested that the tissue kininogen in the inflamed site might participate in the development of potentiative effect of ACE inhibitors on Carr edema.