Collectively, the results show that COX-2 inhibition via intracerebral or peripheral NSAID administration corresponds to diminished retention in hippocampal-dependent spatial memory tasks in adult male rats. Surprisingly, only a handful of studies have investigated the role of COX-2 in normal learning and memory.
However, in the absence of inflammation, COX-2 appears to contribute to constitutive neural function as it is expressed in neurons, regulated by synaptic activity, and integral in hippocampal long-term potentiation (LTP) and depression (LTD). Furthermore, changes in COX-2 expression and activity are associated with pathology-associated cognitive decline. The production of COX-2 by neurons and glia is a common characteristic of neuroinflammation associated with central nervous system injury, neurodegenerative disease, and aging. Since chronic COX-1 inhibition is associated with side effects such as gastrointestinal bleeding and ulcers, COX-2 inhibition became a mainstay therapy in treatment for rheumatoid arthritis, osteoarthritis, and other chronic inflammatory conditions. In contrast, COX-2 is often considered an inducible isoform and a principal contributor to peripheral inflammation via production of prostaglandin E2 (PGE 2). COX exists in two isoforms: COX-1 appears to be constitutively expressed in many tissues and is responsible for homeostatic production of prostanoids. The principal target of NSAIDs is cyclooxygenase (COX), the requisite enzyme for synthesis of potent lipid mediators called prostanoids.
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for the treatment of peripheral pain and inflammation, with millions of people using over-the-counter and prescription NSAIDs daily.
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