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M. FRESNO Y COLS. AN. R. ACAD. NAC. FARM

Surprisingly, COX-1 KO mice show no gastric pathology and are
resistant to classical NSAIDs-induced gastric ulceration. COX-1 deficient
mice show reduced platelet aggregation that is consistent with the fact
that platelets express only COX-1. However, those mice also have a
decreased arachidonic acid-induced inflammation indicating a role of this
enzyme in inflammatory responses (27).

FIGURE 2.- Cyclooxygenases are the target of non-steroidal anti-inflammatory drugs
(NSAIDs). NSAIDs exert their anti-inflammatory and analgesic actions through

inhibition of COX enzymatic activity. Classical non selective NSAIDs, such as Aspirin
and Indomethacin inhibit COX-1 and COX-2 isoforms at standard doses. Unwanted side

effects of these drugs such as gastrointestinal and renal toxicity occurs through the
inhibition of the COX-1 –dependent production of prostanoids involved in physiological

functions. The ability of NSAIDs to inhibit COX-2 activity explains their therapeutic
effects as anti-inflammatory drugs. Newer NSAIDs belonging to the family of Coxibs,
such as Celecoxib and Rofecoxib, with high selectivity against COX-2, have been shown

to exhibit potent anti-inflammatory properties without causing gastric toxicity.

Subcellular location of COX isoenzymes may also be important in
determining their distinct functions. Thus, COX-1 has been mainly

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