e brain and renal cortex(TABLE 3). COX-2 is induced primarily by infla mmatory cytokines during tissue injury, and thus generates the prostaglandins that cause pain and inflammation. Therefore, the therapeutic activity of NSAIDs should be due to COX-2 inhibition, while toxicity may be primarily the result of COX-1 inhibition. COX-1 appears to have no role in producing pain or inflammation, since COX-2 specific inhibitors have analgesic and anti-inflammatory activity equivalent to those of older NSAIDs< ÀúÀÛ±ÇÀÚ © ¾à±¹½Å¹® ¹«´ÜÀüÀç ¹× Àç¹èÆ÷±ÝÁö > |
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