Article(id=1291704983813120072, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.17.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1743091200000, receivedDateStr=2025-03-28, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896066859, onlineDateStr=2026-08-05, pubDate=1758038400000, pubDateStr=2025-09-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896066859, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896066859, creator=13701087609, updateTime=1785896066859, updator=13701087609, issue=Issue{id=1291704771212234905, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='17', pageStart='2401', pageEnd='2550', issueExtLink='null', onlineDate='null', pubDate='1758038400000', pubDateStr='2025-09-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896016147, creator='13701087609', updateTime=1785896900366, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708479866164175, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708479866164176, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2483, endPage=2488, ext={EN=ArticleExt(id=1291704985511813193, articleId=1291704983813120072, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the aggravating effect and mechanism of hyperuricemia on acetaminophen-induced liver injury, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effect and potential mechanism of hyperuricemia (HUA) on acetaminophen (APAP)-induced liver injury.
Methods Male mice were randomly divided into four groups: group A (control), group B [establishment of a hyperuricemia (HUA) model], group C (administered by oral gavage at a dose of 300 mg·kg-1 APAP), and group D (establishment of a HUA model combined with administered by oral gavage at a dose of 300 mg·kg-1 APAP). The HUA model was established by intraperitoneal injection of potassium oxonate (350 mg·kg-1) and gavage of xanthine (450 mg·kg-1) for 14 consecutive days. On day 13, mice in group C and group D received APAP via gavage. All mice were sacrificed 24 h later. Serum levels of uric acid (UA), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined by biochemical analyzer. Liver histopathology was evaluated by hematoxylin-eosin (H&E) staining. Levels of malondialdehyde (MDA), reactive oxygen species (ROS), glutathione (GSH), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in liver tissues were measured using commercial kits. Immunofluorescence was used to detect the relative expression of nuclear factor erythroid 2-related factor 2 (Nrf2).
Results The serum uric acid levels in the group A, group B, group C and group D were (186.20±15.61), (521.50±56.81), (325.20±31.74) and (682.00±49.51) μmol·L-1, respectively; the liver coefficients were (4.51±0.14)%, (4.77±0.23)%, (4.98±0.21)%, and (5.51±0.30)%, respectively; the serum ALT levels were (55.80±15.86), (78.09±10.92), (27 688.81±7 166.01), and (34 571.89±7 793.74) U·L-1, respectively; the AST levels were (159.90±29.72), (143.70±26.46), (10 880.00±4 291.01), and (19 824.84±7 874.64) U·L-1, respectively; the hepatic MDA contents were (5.42±0.38), (7.77±0.32), (6.07±0.31), and (9.08±0.36) mol·g-1·prot-1, respectively; the ROS contents were (28.09±3.52), (39.67±2.70), (32.22±4.71), and (45.67±2.71) μg·g-1·prot-1, respectively; the GSH levels were (2.47±0.27), (1.72±0.16), (2.24±0.16), and (1.37±0.11) μg·g-1·prot-1, respectively; the IL-1β contents were (22.16±0.88), (31.74±1.82), (25.35±1.07), and (38.82±1.68) μg·g-1·prot-1, respectively; the TNF-α contents were (114.90±10.60), (180.20±3.72), (142.20±4.69), and (228.10±17.33) μg·g-1·prot-1, respectively; the relative protein expression of Nrf2 were 218.30±5.16, 63.60±29.02, 100.80±23.60, and 9.31±8.83, respectively. The indices in groups B and C were significantly different from those in group A, and the indices in group D were significantly different from those in group C, with all differences showing statistical significance (P<0.05).
Conclusion In the hyperuricemia (HUA) mouse model, the liver damage induced by acetaminophen (APAP) is aggravated, and this effect may be related to the downregulation of NRF2 expression.
, authors=Hao-lin HUANG, Meng-ting LI, You-xi ZHOU, Shuai-shuai ZHANG, Jian-xin PANG, Ting WU, authorsList=Hao-lin HUANG, Meng-ting LI, You-xi ZHOU, Shuai-shuai ZHANG, Jian-xin PANG, Ting WU, authorCompany=null, correspAuthors=Ting WU, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291704985981575242, articleId=1291704983813120072, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=高尿酸血症加剧对乙酰氨基酚所致肝损伤的作用和机制研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探索高尿酸血症（HUA）对对乙酰氨基酚（APAP）诱导的肝损伤的作用及潜在机制。
方法 将雄性小鼠随机分为A组（空白对照组）、B组（构建HUA模型）、C组（灌胃给予300 mg·kg-1 APAP）及D组（构建HUA模型+灌胃给予300 mg·kg-1 APAP）4组。通过持续14 d腹腔注射氧嗪酸钾（350 mg·kg-1）联合灌胃次黄嘌呤（450 mg·kg-1）制备HUA小鼠模型，在第13 d给C组和D组小鼠灌胃APAP，并于24 h后处死小鼠。用生化分析仪检测各组小鼠的血清尿酸（UA）、血清谷丙转氨酶（ALT）和谷草转氨酶（AST）水平，用苏木精-伊红（H&E）染色法评估小鼠肝组织病理状态，用试剂盒检测肝组织脂质过氧化损伤标志物丙二醛（MDA）、氧化应激损伤标志物活性氧（ROS）、肝功能标志物谷胱甘肽（GSH）、炎症损伤因子白介素1-β（IL-1β）和肿瘤坏死因子-α（TNF-α）水平，用免疫荧光分析法检测核因子E2相关因子2（Nrf2）的蛋白相对表达水平。
结果 A组、B组、C组和D组的UA含量分别为（186.20±15.61）、（521.50±56.81）、（325.20±31.74）和（682.00±49.51）μmol·L-1；肝系数分别为（4.51±0.14）%、（4.77±0.23）%、（4.98±0.21）%和（5.51±0.30）%；血清ALT水平分别为（55.80±15.86）、（78.09±10.92）、（27 688.81±7 166.01）和（34 571.89±7 793.74）U·L-1; AST水平分别为（159.90±29.72）、（143.70±26.46）、（10 880.00±4 291.01）和（19 824.84±7 874.64）U·L-1; MDA含量分别为（5.42±0.38）、（7.77±0.32）、（6.07±0.31）和（9.08±0.36）μmol·g-1·prot-1; ROS含量分别为（28.09±3.52）、（39.67±2.70）、（32.22±4.71）和（45.67±2.71）μg·g-1·prot-1; GSH含量分别为（2.47±0.27）、（1.72±0.16）、（2.24±0.16）和（1.37±0.11）μg·g-1·prot-1; IL-1β含量分别为（22.16±0.88）、（31.74±1.82）、（25.35±1.07）和（38.82±1.68）μg·g-1·prot-1; TNF-β分别为（114.90±10.60）、（180.20±3.72）、（142.20±4.69）和（228.10±17.33）μg·g-1·prot-1; Nrf2蛋白相对表达水平分别为218.30±5.16、63.60±29.02、100.80±23.60和9.31±8.83; B组和C组的上述指标与A组相比，D组的上述指标与C组相比，在统计学上差异均有统计学意义（均P<0.05）。
结论 在小鼠高尿酸血症模型中，对乙酰氨基酚引起的肝损伤作用加剧，其作用机制可能与其下调NRF2的表达有关。
, authors=黄浩林, 黎梦婷, 周佑熙, 张帅帅, 庞建新, 吴婷, authorsList=黄浩林, 黎梦婷, 周佑熙, 张帅帅, 庞建新, 吴婷, authorCompany=null, correspAuthors=吴婷, authorNote=
黄浩林（2003-），男，本科，主要从事高尿酸血症方面的研究
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