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STW 5 is effective against nonsteroidal anti-inflammatory drugs induced gastro-duodenal lesions in rats 被引量:1
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作者 Mohamed T Khayyal Walaa Wadie +4 位作者 Enas a abd El-Haleim kawkab a ahmed Olaf Kelber Ramy M ammar Heba abdel-aziz 《World Journal of Gastroenterology》 SCIE CAS 2019年第39期5926-5935,共10页
BACKGROUND Proton pump inhibitors are often used to prevent gastro-intestinal lesions induced by nonsteroidal anti-inflammatory drugs.However,they are not always effective against both gastric and duodenal lesions and... BACKGROUND Proton pump inhibitors are often used to prevent gastro-intestinal lesions induced by nonsteroidal anti-inflammatory drugs.However,they are not always effective against both gastric and duodenal lesions and their use is not devoid of side effects.AIM To explore the mechanisms mediating the clinical efficacy of STW 5 in gastroduodenal lesions induced by nonsteroidal anti-inflammatory drugs(NSAIDs),exemplified here by diclofenac,in a comparison to omeprazole.METHODS Gastro-duodenal lesions were induced in rats by oral administration of diclofenac(5 mg/kg)for 6 successive days.One group was given concurrently STW 5(5 mL/kg)while another was given omeprazole(20 mg/kg).A day later,animals were sacrificed,stomach and duodenum excised and divided into 2 segments:One for histological examination and one for measuring inflammatory mediators(tumor necrosis factorα,interleukins-1βand 10),oxidative stress enzyme(heme oxygenase-1)and apoptosis regulator(B-cell lymphoma 2).RESULTS Diclofenac caused overt histological damage in both tissues,associated with parallel changes in all parameters measured.STW 5 and omeprazole effectively prevented these changes,but STW 5 superseded omeprazole in protecting against histological damage,particularly in the duodenum.CONCLUSION The findings support the therapeutic usefulness of STW 5 and its superiority over omeprazole as adjuvant therapy to NSAIDs to protect against their possible gastro-duodenal side effects. 展开更多
关键词 DICLOFENAC STW 5 OMEPRAZOLE Gastro-intestinal LESIONS Inflammation
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