Related Experiment Video
Updated: May 2, 2026
Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine
Published on: July 7, 2016
Repurposing piroxicam for antithrombotic and cardiopulmonary protection: Pharmacological rationale and therapeutic
Waseem Khalid1, Arif-Ullah Khan
1Department of Pharmacology, Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 04405, Pakistan.
Background:
Recent research indicates that non-steroidal anti-inflammatory drugs may interfere in coagulation process and platelet aggregation. However, the potential of piroxicam in thrombotic and cardiopulmonary disorders remained unexplored.
Objectives:
To bridge this knowledge gap, the current study was conducted to assess the potential of piroxicam as antithrombotic and cardiopulmonary protective agent using multi-level approaches.
Materials And Methods:
Piroxicam was docked against 16 key proteins involved in thrombotic and cardiopulmonary conditions. Its antiplatelet effect was evaluated by arachidonic acid (AA) and adenosine diphosphate (ADP)-induced aggregation while its effect on coagulation parameters were also evaluated. Cardiopulmonary protective effect in rats was investigated through isoproterenol induced myocardial infarction (MI) and self-embolus induced pulmonary embolism (PE).
Results:
Strong binding interactions were identified, with docking energies of ≥-9.0 kcal/mol noted for cyclooxygenase (COX) 1, glycopotein-IIb/IIIa, antithrombin-III, COX-2, and nuclear factor Kappa-B (NFkB). Piroxicam significantly inhibited AA and ADP-induced platelet aggregation (IC50: 0.68 and 24.9 μM) and also prolonged the prothrombin, activated partial thromboplastin, thrombin, and clot lysis time. Piroxicam markedly and in a dose-related manner lowered MI and PE associated serum markers in experimental rats. Piroxicam further safeguarded cardiac and pulmonary tissues from infarction and histopathological injury through the suppression of oxidative imbalance and inflammatory activity. This protective outcome was also due to reduced expression of tissue necrosis factor-α, NFkB, COX-2, NLRP3, and platelet-derived growth factor-β, verified using immunohistochemistry, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction RT-PCR techniques.
Conclusions:
These results indicate the prophylactic potential of piroxicam in cardiopulmonary thrombotic disorders.
More Related Videos
Related Concept Videos
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
01:23Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
01:27Peripheral Artery Disease III: Interprofessional Care
01:26Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
01:25Cardiopulmonary Resuscitation IV: Pharmacological Management
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...