cyclooxygenases (sīˈ·klō·kˈ·s·je·nāˑ·ss), enzymes that are rate-limiting in the production of thromboxanes and prostaglandins from arachidonic acid. The constitutive form of these proteins is essential for maintaining homeostasis while the indu-cible form is expressed in leukocytes in response to an inflammatory stimulus, resulting in production of prostanoids. The activity of cyclooxygenases is inhibited by antiinflammatory drugs, such as aspirin, and corticosteroids interfere with gene expression of the inducible form of the enzyme.
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This might be due to non-selective inhibition of cyclooxygenases that provides support in the synthesis of prostanoids necessary for generating signals by APCs (Antigen presenting cells) and transmitting these signals to T cells.
cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function.
Cyclooxygenases are known for their role in synthesis of prostaglandins which have gastro protective activity.
Table 2: Expression of renal cyclooxygenases (COX-1 and -2) in rats with PUUO at 9 and 15 weeks (mean ± SEM) [Table omitted]
Comparative pathophysiology and toxicology of cyclooxygenases.
They also discuss in vivo disease models used to study the role of cyclooxygenases in gastrointestinal injury, inflammation, and pain.
The inhibition of various enzymes of the arachidonic acid cascade, among these the lipoxygenases and the cyclooxygenases, might be a possible target.
Lipsky LP, Abramson SB, Crofford L, Dubois RN, Simon LS, Van de Putte LB (1998) The classification of cyclooxygenases inhibitors.
Among the physiological activators of platelet, thromboxane A [sub]2 (TXA [sub]2 ) is the primary one which is conversed from arachidonic acid in the platelets and catalyzed by cyclooxygenase (COX).
Cyclooxygenase (COX), the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids (Sheng et al.

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