针对非甾体抗炎药诱导胃病的氧化应激和炎症:一种可行的治疗方法

K. Sinha, P. Sil
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引用次数: 15

摘要

前列腺素(PG)生物合成、氧化应激、炎症和细胞凋亡的失调在非甾体抗炎药(NSAID)诱导胃病的发病机制中起主要作用。尽管参与这种病理生理状况的潜在分子机制尚不完全清楚,但近年来已经取得了相当大的进展。此外,在寻找安全且经济有效的抗非甾体抗炎药诱导胃病的胃保护剂方面也取得了实质性进展。在这篇文章中,我们简要介绍了nsaid诱导胃病研究领域的当代进展,并希望提供一个简明的观点,重点关注氧化应激和炎症在这种病理生理中的潜在作用。同时,也有针对性地强调了胃保护剂的最新发展趋势。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting oxidative stress and inflammation in NSAIDs induced gastropathy: A plausible therapeutic approach
Deregulation in prostaglandin (PG) biosynthesis, oxidative stress, inflammation, and apoptosis play a major role in the pathogenesis of nonsteroidal anti-inflammatory drug (NSAID)-induced gastropathy. Although the underlying molecular mechanisms involved in this pathophysiological condition is not fully understood, considerable progress has been made in recent years. Also, substantial progress has been made in the search for safe and cost effective gastroprotective agents against NSAID-induced gastropathy. In this article, we briefly describe the contemporary advancement in the field of NSAID-induced gastropathy research and would like to provide a concise view focusing the underlying role of oxidative stress and inflammation in this pathophysiology. Simultaneously, the recent trends in the pursuit of gastroprotective agent have also been highlighted purposely.
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