Astragaloside IV Attenuates Acetaminophen-Induced Liver Injuries in Mice by Activating the Nrf2 Signaling Pathway.
Astragaloside IV Attenuates Acetaminophen-Induced Liver Injuries in Mice by Activating the Nrf2 Signaling Pathway.
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星形镜IV通过激活NRF2信号途径来减轻小鼠乙酰氨基酚诱导的肝损伤。
DOI：
10.3390/molecules23082032
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发表时间：
2018-08-14
期刊：
影响因子：
--
通讯作者：
Liu C
中科院分区：
文献类型：
--
作者：
Li L;Huang W;Wang S;Sun K;Zhang W;Ding Y;Zhang L;Tumen B;Ji L;Liu C
对乙酰氨基酚(APAP)是一种著名的解热止痛药。然而，意外或故意的APAP过量会导致肝损伤，甚至急性肝功能衰竭。黄芪皂苷IV(AS-IV)是从黄芪中分离得到的一种生物活性物质，具有抗氧化和抗炎作用，对消化系统和免疫系统具有保护作用。本研究旨在观察AS-IV预处理对APAP诱导的肝功能衰竭是否具有保护作用。血清丙氨酸/天冬氨酸氨基转移酶(ALT/AST)、肝脏谷胱甘肽(GSH)、丙二醛(MDA)含量及肝脏超氧化物歧化酶(SOD)活性检测结果表明，AS-IV对APAP诱导的肝毒性具有保护作用。肝脏组织学观察进一步证明了AS-IV提供的这种保护作用。AS-IV可逆转AP诱导的促炎细胞因子的增加，包括白介素1β(IL-1β)、白介素6(IL-6)和肿瘤坏死因子α(TWF-α)。Western-blotting分析显示，AS-IV可增强核因子红系相关因子2(NRF2)的转录活性，增强HO-1和还原烟酰胺腺嘌呤二核苷酸磷酸(NAD(P)H)：苯醌氧化还原酶1(NQO1)的表达。AS-IV还可降低海带样ECH相关蛋白-1(Keap1)的表达。综上所述，我们证明AS-IV通过激活Nrf2抗氧化信号通路，对APAP诱导的肝损伤具有较强的保护作用。
Acetaminophen (APAP) is a well-known antipyretic and analgesic drug. However, the accidental or intentional APAP overdose will induce liver injury and even acute liver failure. Astragaloside IV (AS-IV), a bioactive compound isolated from Astragali Radix, has been reported to have protective effects on the digestive and immune systems because of its anti-oxidant and anti-inflammatory properties. This study aims to observe whether AS-IV pretreatment provides protection against APAP-induced liver failure. The results of serum alanine/aspartate aminotransferases (ALT/AST) analysis, hepatic glutathione (GSH), and malondialdehyde (MDA) amounts, and liver superoxide dismutase (SOD) activity showed that AS-IV protected against APAP-induced hepatotoxicity. Liver histological observation further evidenced this protection provided by AS-IV. AS-IV was found to reverse the APAP-induced increased amounts of pro-inflammatory cytokines, including interleukin 1β (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α). Western-blot analysis showed that AS-IV increased the transcriptional activation of nuclear factor erythroid 2-related factor 2 (Nrf2), and enhanced the expression of heme oxygenase 1 (HO-1) and reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase 1 (NQO1) in the presence of APAP. AS-IV also decreased the expression of kelch-like ECH-associated protein-1 (Keap1). In conclusion, we demonstrated that AS-IV exerted a strong protection against APAP-induced hepatotoxicity by activating Nrf2 antioxidant signaling pathways.
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