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Re: دراسه تربط بين استخدام (البروفين) وزيادة نسب الاجهاض.. (Re: محمد ابراهيم قرض)
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الاخ محمد تحياتى القائمين على امر الدراسه لم يوضحوا بعد لماذا البروفين بالذات وعلى غير الNSAIDs الاخرى..صحيح ان كل هذه العائله تعمل على تثبيط الProstaglandins وكما تعلم فان الprotaglandins تستخدم كمواد مجهضه ومن هنا فان تثبيطها لايكون سبا للاجهاض على الاقل نظريا.. لكن هنالك خصائص تميز بعض الNSAIDs عن بعضها البعض وقد تكرمت بذكر احدها فيما يتعلق بال Brufen ولاباس من ايراد كيفية عمل البروفين ...فى الختام سوف اقوم بمراسلة المركز الذى قام بالدراسه وساقوم بافادتكم بكل جديد ودمتم..
Quote: Mechanism of action Nonsteroidal anti-inflammatory drugs such as ibuprofen work by inhibiting the enzyme cyclooxygenase (COX), which converts arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever) and to thromboxane A2 (which stimulates platelet aggregation, leading to the formation of blood clots). Like aspirin, indomethacin, and most other NSAIDs,[citation needed] ibuprofen is considered a nonselective COX inhibitor; that is, it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to be achieved mainly through inhibition of COX-2, whereas inhibition of COX-1 would be responsible for unwanted effects on platelet aggregation and the gastrointestinal tract.[32] However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain and different compounds cause different degrees of analgesia and gastric damage.[33] In order to achieve the beneficial effects of ibuprofen and other NSAIDS without gastrointestinal ulceration and bleeding, selective COX-2 inhibitors were developed to inhibit the COX-2 isoform without inhibition of COX-1.
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(عدل بواسطة د.محمد بابكر on 09-07-2011, 03:04 PM) (عدل بواسطة د.محمد بابكر on 09-07-2011, 04:12 PM)
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