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Toxicity of triptolide and the molecular mechanisms involved
Biomedicine & Pharmacotherapy ( IF 6.9 ) Pub Date : 2017-04-10 , DOI: 10.1016/j.biopha.2017.04.003 Chen Xi 1 , Shaojun Peng 2 , Zhengping Wu 2 , Qingping Zhou 3 , Jie Zhou 2
Biomedicine & Pharmacotherapy ( IF 6.9 ) Pub Date : 2017-04-10 , DOI: 10.1016/j.biopha.2017.04.003 Chen Xi 1 , Shaojun Peng 2 , Zhengping Wu 2 , Qingping Zhou 3 , Jie Zhou 2
Affiliation
Triptolide (TP), a major active and toxic ingredient isolated from the traditional Chinese herb Hook f. (TWHF). A widespread application of TP raises the question on the safety of its use in clinical settings. The metabolism of TP is mediated by hepatic cytochrome P450s, and a strong correlation exists between TP toxicity and CPY3A. Toxicity of TP and the molecular mechanisms of its toxic effects have been studied in recent years. Studies have demonstrated that TP exposure results in injury of various organs, including the liver, kidney, testes, ovary, and heart in animals and even in humans, according to clinical case reports. Moreover, on the cellular level, TP has been reported to be associated with diverse toxic effects, encompassing membrane damage, mitochondrial disruption, metabolism dysfunction, endoplasmic reticulum stress, oxidative stress, apoptosis and autophagy. This review presents an overview of the current findings related to TP toxicity with an emphasis on biological targets and the molecular mechanisms that may be involved, thus providing a systematic understanding of the mechanisms by which TP affects cells and tissues and .
中文翻译:
雷公藤甲素的毒性及其分子机制
雷公藤甲素 (TP) 是从传统中药胡克 f 中分离出来的主要活性成分和有毒成分。 (TWHF)。 TP 的广泛应用引发了其在临床环境中使用的安全性问题。 TP的代谢由肝细胞色素P450介导,TP毒性与CPY3A之间存在很强的相关性。近年来,人们对TP的毒性及其毒性作用的分子机制进行了研究。根据临床病例报告,研究表明,TP 暴露会导致动物甚至人类的各种器官损伤,包括肝脏、肾脏、睾丸、卵巢和心脏。此外,在细胞水平上,据报道TP与多种毒性作用有关,包括膜损伤、线粒体破坏、代谢功能障碍、内质网应激、氧化应激、细胞凋亡和自噬。本综述概述了当前与 TP 毒性相关的研究结果,重点关注可能涉及的生物靶点和分子机制,从而提供了对 TP 影响细胞和组织的机制的系统理解。
更新日期:2017-04-10
中文翻译:
雷公藤甲素的毒性及其分子机制
雷公藤甲素 (TP) 是从传统中药胡克 f 中分离出来的主要活性成分和有毒成分。 (TWHF)。 TP 的广泛应用引发了其在临床环境中使用的安全性问题。 TP的代谢由肝细胞色素P450介导,TP毒性与CPY3A之间存在很强的相关性。近年来,人们对TP的毒性及其毒性作用的分子机制进行了研究。根据临床病例报告,研究表明,TP 暴露会导致动物甚至人类的各种器官损伤,包括肝脏、肾脏、睾丸、卵巢和心脏。此外,在细胞水平上,据报道TP与多种毒性作用有关,包括膜损伤、线粒体破坏、代谢功能障碍、内质网应激、氧化应激、细胞凋亡和自噬。本综述概述了当前与 TP 毒性相关的研究结果,重点关注可能涉及的生物靶点和分子机制,从而提供了对 TP 影响细胞和组织的机制的系统理解。