| 张真真,曲爱娟,王艳.过氧化物酶体增殖物激活受体α在对乙酰氨基酚肝损伤的研究进展[J].安徽医药,2018,22(12):2279-2282. |
| 过氧化物酶体增殖物激活受体α在对乙酰氨基酚肝损伤的研究进展 |
| Recent advance in the role of peroxisome proliferator-activated receptor α in acetaminophen-induced hepatotoxicity |
| 投稿时间：2017-07-31 |
| DOI： |
| 中文关键词: 对乙酰氨基酚 肝毒性 过氧化物酶体增殖物激活受体α 氧化应激 炎症 |
| 英文关键词: Acetaminophen Hepatotoxicity PPAR α Oxidative stress Inflammation |
| 基金项目:国家自然科学基金资助项目(81300312,81370521和81302157)；中国肝炎防治基金资助项目(CFHPC20132028) |
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| 中文摘要: |
| 对乙酰氨基酚(Acetaminophen,APAP)药物过量是我国及欧美国家急性肝衰竭的常见原因之一。正常剂量的APAP约90%以上经过肝内Ⅱ相代谢酶UDP-葡萄糖醛酸转移酶(UGT)和磺基转移酶(SULT)转化为无毒的葡萄糖醛酸盐或硫酸盐从肾脏和胆汁排泄,10%以下通过肝内I相代谢酶细胞色素P450酶转化为活性代谢产物N-乙酰基-对-苯醌亚胺(NAPQI),NAPQI随后在谷胱甘肽-S-转移酶(GST)的作用下转化为无毒的化合物。当APAP过量时,NAPQI蓄积,继而引起肝损伤。代谢性核受体过氧化物酶体增殖物激活受体α (Peroxisome proliferator activated receptor ,PPARα),作为核受体超家族成员之一,参与肝脏脂质代谢及多种生物转化过程,多个研究表明PPARα激动剂可保护APAP引起的肝损伤,该文将对PPARα在APAP引起的肝损伤中的作用及机制进行综述,以期为APAP诱导的肝损伤提供潜在的治疗靶点。 |
| 英文摘要: |
| Acetaminophen (APAP) overdose is one of the main causes for acute liver failure.Most of the drugs are catalyzed by UDP-glucuronosyltransferases (UGT) and sulfotransferases (SULT) and then excreted in the urine.A small percentage is converted by cytochrome P450 enzymes to a reactive intermediate N-acetyl-p-benzoquinone imine (NAPQI),which can bind to proteins and deplete glutathione (GSH),leading to hepatotoxicity.Peroxisome proliferator-activated receptor α(PPAR α) belongs to nuclear receptor superfamily.Activation of PPAR α by its ligands controls fatty acid metabolism and regulates many biological transformation processes.Increasing evidence shows that PPAR α activation may protect against APAP-induced liver toxicity.In this review,we will summarize the role of PPAR α in APAP-induced hepatotoxicity and the underlying mechanisms,thus providing potential therapeutic target for this disease. |
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