TY - JOUR AU - Patel, Mihir K. AU - Chaudagar, Kiranj K. AU - Mehta, Anita A. PY - 2018/04/01 Y2 - 2024/03/28 TI - ROLE OF NITRIC OXIDE (NO) IN CAPSAICIN MEDIATED ANTI-PLATELET ACTIVITY IN IN VITRO, IN VIVO, EX-VIVO MODEL OF PLATELET AGGREGATION ASSAY AND ARTERIAL THROMBOSIS IN RAT: POTENTIAL THERAPEUTIC TARGET? JF - International Journal of Pharmacy and Pharmaceutical Sciences JA - Int J Pharm Pharm Sci VL - 10 IS - 4 SE - Original Article(s) DO - 10.22159/ijpps.2018v10i4.22474 UR - https://journals.innovareacademics.in/index.php/ijpps/article/view/22474 SP - 44-48 AB - <p><strong>Objective: </strong>Although recent advances in the treatment of congestive heart disease, mortality among patients' remains a questionable remark. Therefore, we evaluated the role of capsaicin on <em>in vitro</em> and <em>ex vivo</em> platelet aggregation induced by Adenosine Di-Phosphate (ADP) as well as in <em>in</em><em> vivo</em> thrombosis models and role of NO, K<sub>ATP</sub> was also identified in the capsaicin-induced anti-platelet animal model as well as <em>in vivo</em> model of arterial thrombosis.</p><p><strong>Methods: </strong>According to body weight wistar rats were divided into five groups. Group I and Group II was treated with saline and capsaicin (3 mg/kg, i. v), while animals from Group III were treated with N(ω)-nitro-L-arginine methyl ester (L-NAME) (30 mg/kg, i. v) 30 min before administration of capsaicin (3 mg/kg, i. v). Group IV animals were treated with glibenclamide (10 mg/kg,i. v) 30 min before administration of capsaicin (3 mg/kg, i. v). Group V was considered as a positive control and administered clopidogrel (30 mg/kg, p. o). Animals were subjected for <em>in vitro</em>, <em>ex-vivo</em> platelet aggregation assay. ADP (30µM) was utilized as an aggregating agent in these experiments. After these assays; animals of each group were subjected for subaqueous tail bleeding time in a rat model and FeCl<sub>3</sub>-induced arterial thrombosis model in rats.</p><p><strong>Results: </strong>In ADP-induced <em>in vitro</em> platelet aggregation, a significant reduction in % platelet aggregation was observed at 50µM (64.35±4.641) and 100µM (52.72±4.192) concentration of capsaicin as compared to vehicle control (85.82±3.716). Capsaicin (3 mg/kg, i. v) also showed a significant reduction (49.53±4.075) in <em>ex-vivo</em> ADP-induced platelet aggregation as compared to vehicle control (89.38±2.057). In FeCl<sub>3</sub> induced arterial thrombosis model, Capsaicin (3 mg/kg, i. v) exhibited an increase in time to occlusion in this rodent model and presence of the L-NAME and glibenclamide had inhibited the activity of capsaicin.</p><p><strong>Conclusion: </strong>In our study, capsaicin (50 µM, 100µM) exhibited potent anti-platelet activity in ADP-induced platelet aggregation, similarly capsaicin exhibited significant anti-platelet action in the <em>ex-vivo</em> study. Moreover, the presence of L-NAME and glibenclamide inhibited the anti-thrombotic and anti-platelet action of capsaicin. Therefore, it was concluded that NO and K<sub>ATP</sub> may be involved in the anti-thrombotic action of capsaicin.</p> ER -