Inhibition of cyclooxygenase type 1 and 2 enzyme by aqueous extract of elaegnus angustifolia in mice

Introduction: It has been shown that the extract of Elaeagnus angustifolia can inhibit inflammation and pain induced by formalin in mice and rats. The aim of the present study is to reach evaluations of possible cellular and molecular mechanisms of Elaeagnus angustifolia extract in reducing pain and inflammation through examining the extract ability for inhibition of cyclooxygenase [Cox] type 1 and 2 enzymes and corticosterone release from adrenal glands in mice. Methods: Male Swiss Webster mice were evaluated through the injection of 2 µliters to the plantar part of right foot. Elaeagnus angustifolia extract was injected to the animals 30 minutes before formalin. In order to evaluate the mechanism of extract, naloxone and memantine were administered intrapretonealy 30 minutes before the extract administration. In separate groups, after injection of extract, blood samples were taken from animals and corticosterone concentrations were measured. In an in vitro study the effect of extract on the activity of cyclooxygenase type 1 and 2 was assessed. Results: the research data showed the ineffectiveness of the extract on acute phase of pain induced by formalin but it completely inhibits the chronic phase. Naloxone and Memantine administration had no effect on the efficacy of extract in the chronic phase. Also the extract administration did not increase the plasma concentration of corticosterone in mice, but in vitro inhibited Cox1 and Cox 2 enzymes. Discussion: These results indicate that Elaeagnus angustifolia extract probably reducesww pain and inflammation caused by formalin in mice by inhibiting cyclooxygenase type 1 and 2 enzymes

[ neuroprotective effect of cannabinoid receptor agonist [WIN55,212-2] in paraoxon induced neurotoxicity in PC12 cells and N-methyl-D-aspartate receptor interaction]

Considering that cannabinoids protect neurons against neurodegeneration, in this study, the neuroprotective effect of WIN55,212-2 in paraoxon induced neurotoxicity in PC12 cells and the role of the N-methyl-D-aspartate [NMDA] receptor were evaluated. In this study PC12 cells were maintained in Dulbecco's modified eagle's medium [DMEM+F12] culture medium supplemented with 10% fetal bovine serum. The cells were treated with paraoxon [200 micro M] in the presence or absence of WIN55,212-2 [0.1 micro M], NMDA receptor agonist NMDA [100 micro M], cannabinoid receptor antagonist AM251 and NMDA receptor antagonist MK801 [1 micro M] at 15 minutes intervals. After 48 hours of exposure, cellular viability and protein expression of the CB1 receptor were evaluated in PC12 cells. Following the exposure of PC12 cells to paraoxon [200 micro M], a reduction in cell survival and protein level of the CB1 receptor was observed [p<0.01]. Treatment of the cells with WIN55,212-2 [0.1 micro M] and NMDA [100 micro M] prior to paraoxon exposure significantly elevated cell survival and protein level of the CB1 receptor [p<0.01]. Also, AM251 [1 micro M] did not inhibit the cell survival and protein level of the CB1 receptor increase induced by WIN55,212-2 [p<0.001]. However, MK801 [1 micro M] did inhibit cell survival and protein expression of the CB1 receptor increase induced by NMDA [p<0.001]. The results indicate that WIN55,212-2 and NMDA protect PC12 cells against paraoxon induced toxicity. In addition, the neuroprotective effect of WIN55,212-2 and NMDA was cannabinoid receptor-independent and NMDA receptor dependent, respectively