ABSTRACT
Inammation is dened as a complex biological response of vascular tissues to harmful stimuli, such as pathogens, damage cells, or irritants characterized by local redness, swelling, joint pain, heat, and loss of joint function [1]. A large number of chemical mediators such as kinins, eicosanoids, complement proteins, histamine, and monokines regulate these inammatory manifestations. Inammation is either acute or chronic. Acute inammation may be associated with an initial response of the body to harmful stimuli, and failure of acute inammation to resolve may predispose to autoimmunity, chronic dysplastic inammation, and excessive tissue damage. Chronic inammation is an inammatory response that is out of proportion, resulting in damage to the body. Prostaglandins (PGs), prostacyclins, and thromboxanes play a key role in the generation of the inammatory response, pain, and platelet aggregation, and they are generated by the action of cyclooxygenase (COX) isoenzyme. Chronic inammation causes many advanced aged diseases such as heart attack, Alzheimer’s disease, and cancer [2]. Nonsteroidal anti-inammatory drugs (NSAIDs) are the most commonly used drugs to prevent and treat inammation and/or postoperative pain [3]. These drugs block PG production by attenuating COX-1 and COX-2 enzyme activity. The long-term use of steroidal anti-inammatory drugs (SAIDs) and NSAIDs causes adverse side effects and also damages the human biological systems such as the digestive (specically the liver and gastrointestinal tract), renal, and cardiovascular systems [4-6]. Therefore, there is an urgent need to develop new, safe, potent, nontoxic anti-inammatory drugs.
