Article(id=1291707091127919136, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.21.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1747152000000, receivedDateStr=2025-05-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896569281, onlineDateStr=2026-08-05, pubDate=1763308800000, pubDateStr=2025-11-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896569281, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896569281, creator=13701087609, updateTime=1785896569281, updator=13701087609, issue=Issue{id=1291706987964822180, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='21', pageStart='3001', pageEnd='3150', issueExtLink='null', onlineDate='null', pubDate='1763308800000', pubDateStr='2025-11-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896544684, creator='13701087609', updateTime=1785896721343, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707729324826977, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707729324826978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3054, endPage=3060, ext={EN=ArticleExt(id=1291707091589292577, articleId=1291707091127919136, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of Gallic acid on liver tissue damage in autoimmune hepatitis mice by adjusting the AMPK/ACC signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effect of Gallic acid on liver tissue damage in autoimmune hepatitis (AIH) mice by adjusting adenosine monophosphate-activated protein kinase (AMPK) / acetyl-coa carboxylase (ACC) signaling pathway.
Methods An AIH mouse model was established by injecting 15 mg·kg-1 concanavalin A through the tail vein. The mice were randomly divided into model group, low-dose experimental group (50 mg·kg-1), high-dose experimental group (100 mg·kg-1), AMPK inhibitor group (5 μmol·L-1), gallic acid + AMPK inhibitor group and normal mice group with the same volume of phosphate-buffered solution as control group. After the intervention, the automatic biochemical analyzer was used to analyze glutamic pyruvic transaminase (GPT), the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in liver homogenate were detected by enzyme-linked immunosorbent assay (ELISA), and the levels of interleukin (IL)-10, IL-6 and tumor necrosis factor (TNF-α) in serum supernatant were also measured. The histopathological changes were detected by the hematoxylin-eosin (HE) staining method; the apoptosis status was examined by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. The relative expression levels of phosphorylated (p-) AMPK/AMPK, Bcl-2 related X protein (Bax), B-cell lymphoma/leukemia-2 protein (Bcl-2) and ACC protein were detected by Western blotting.
Results The glutamic-oxalacetic transaminase (GOT) levels in control group, model group, low-dose experimental group, high-dose experimental group, AMPK inhibitor group and high-dose experimental+AMPK inhibitor group were (82.05±8.31), (210.20±21.14), (135.26±14.64), (91.02±9.21), (308.15±30.85) and (129.84±13.08) U·L-1, respectively; the GPT levels were (50.23±5.11), (324.85±33.25), (152.34±15.48), (88.64±8.95), (482.62±50.02) and (148.85±15.02) U·L-1, respectively; the TNF-α levels were (41.06±4.37), (149.85±15.28), (88.39±8.97), (51.06±5.21), (267.85±27.18) and (154.62±15.68) pg·mL-1, respectively; the IL-6 levels were (48.42±4.92), (134.52±13.58), (75.42±7.61), (57.85±5.81), (215.84±21.98) and (78.62±7.98) pg·mL-1, respectively; the IL-10 levels were (486.52±49.02), (188.72±19.08), (318.54±32.08), (445.67±45.11), (114.21±11.94) and (324.15±32.67) pg·mL-1, respectively; the SOD levels were (48.26±4.99), (19.52±2.11), (32.25±3.44), (44.21±4.57), (11.37±1.21) and (31.24±3.22) U·mg-1, respectively; the MDA levels were (0.28±0.03), (0.84±0.09), (0.56±0.06), (0.31±0.04), (1.31±0.15) and (0.64±0.07) nmol·mg-1, respectively; the tissue pathological scores were 0, 2.64±0.27, 2.27±0.24, 1.22±0.14, 3.54±0.36 and 2.19±0.23, respectively; the apoptosis rates were (5.24±0.54)%, (23.62±2.44)%, (16.42±1.72)%, (8.52±0.89)%, (34.85±3.61)% and (17.06±1.75)%, respectively. The above indexes of model group were compared with those of control group; low-dose and high-dose experimental group were compared with those of model group and high-dose experimental+AMPK inhibitor group were compared with those of high-dose experimental group, there were statistically significant differences (all P<0.05).
Conclusion Gallic acid can inhibit the inflammatory response and oxidative stress level in AIH mice, reduce cell apoptosis, improve liver function, alleviate liver tissue pathological damage, down-regulate Bax and ACC expression, up-regulate p-AMPK/AMPK and Bcl-2 expression; the AMPK inhibitor reverses the protective effect of high-dose gallic acid on AIH mice. Gallic acid activates the AMPK/ACC signaling pathway to alleviate liver tissue damage in AIH mice.
, authors=Gao-bo LI
1a, Ting WANG
1b, Yu-zhang HUO
2, ADILAI
1a, Yong-rong SONG
1a, Jian-hong LÜ
1a, Yu-hua ZHANG
1a, authorsList=Gao-bo LI, Ting WANG, Yu-zhang HUO, ADILAI, Yong-rong SONG, Jian-hong LÜ, Yu-hua ZHANG, authorCompany=null, correspAuthors=Ting WANG, 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=1291707092222632482, articleId=1291707091127919136, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=没食子酸调节AMPK/ACC信号通路对自身免疫性肝炎小鼠肝组织损伤的研究, 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 探讨没食子酸调节腺苷酸活化蛋白激酶（AMPK）/乙酰辅酶A羧化酶（ACC）信号通路对自身免疫性肝炎（AIH）小鼠肝组织损伤的影响。
方法 通过尾静脉注射15 mg·kg-1刀豆蛋白A构建AIH小鼠模型，随机分为模型组、低剂量实验组（50 mg·kg-1）、高剂量实验组（100 mg·kg-1）组、AMPK抑制剂组（5 μmol·L-1）组和没食子酸+AMPK抑制剂组，并以等体积的磷酸缓冲液处理的正常小鼠为对照组。干预结束后，自动生化分析仪分析谷丙转氨酶（GPT）等水平，用酶联免疫吸附测定法（ELISA）法检测肝匀浆中丙二醛（MDA）和超氧化物歧化酶（SOD）水平，血清上清液中白细胞介素（IL）-10、IL-6和肿瘤坏死因子（TNF-α）水平；用苏木精-伊红（HE）法检测组织病理学变化；用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法检测细胞凋亡情况；用蛋白质印迹法检测磷酸化（p-）AMPK/AMPK、Bcl-2相关X蛋白（Bax）、B细胞淋巴瘤/白血病-2蛋白（Bcl-2）和ACC蛋白相对表达水平。
结果 对照组、模型组、低剂量实验组、高剂量实验组、AMPK抑制剂组和高剂量实验+AMPK抑制剂组谷草转移酶（GOT）分别为（82.05±8.31）、（210.20±21.14）、（135.26±14.64）、（91.02±9.21）、（308.15±30.85）和（129.84±13.08）U·L-1，GPT分别为（50.23±5.11）、（324.85±33.25）、（152.34±15.48）、（88.64±8.95）、（482.62±50.02）和（148.85±15.02）U·L-1，TNF-α分别为（41.06±4.37）、（149.85±15.28）、（88.39±8.97）、（51.06±5.21）、（267.85±27.18）和（154.62±15.68）pg·mL-1，IL-6分别为（48.42±4.92）、（134.52±13.58）、（75.42±7.61）、（57.85±5.81）、（215.84±21.98）和（78.62±7.98）pg·mL-1，IL-10分别为（486.52±49.02）、（188.72±19.08）、（318.54±32.08）、（445.67±45.11）、（114.21±11.94）和（324.15±32.67）pg·mL-1，SOD分别为（48.26±4.99）、（19.52±2.11）、（32.25±3.44）、（44.21±4.57）、（11.37±1.21）和（31.24±3.22）U·mg-1，MDA分别为（0.28±0.03）、（0.84±0.09）、（0.56±0.06）、（0.31±0.04）、（1.31±0.15）和（0.64±0.07）nmol·mg-1，组织病理评分分别为0、2.64±0.27、2.27±0.24、1.22±0.14、3.54±0.36和2.19±0.23，凋亡率分别为（5.24±0.54）%、（23.62±2.44）%、（16.42±1.72）%、（8.52±0.89）%、（34.85±3.61）%和（17.06±1.75）%，模型组的上述指标与对照组比较、低、高剂量实验组的上述指标与模型组比较及高剂量实验+AMPK抑制剂组的上述指标与高剂量实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 没食子酸可以抑制AIH小鼠炎症反应及氧化应激水平，减少细胞凋亡，改善肝功能，减轻肝组织病理损伤，下调Bax和ACC表达，上调p-AMPK/AMPK和Bcl-2表达，AMPK抑制剂逆转了高剂量没食子酸对AIH小鼠的保护作用。没食子酸激活AMPK/ACC信号通路减轻AIH小鼠肝组织损伤。
, authors=李高波
1a, 王婷
1b, 霍昱章
2, 阿迪莱
1a, 宋永蓉
1a, 吕健宏
1a, 张煜华
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李高波（1980-），男，主治医师，主要从事感染疾病相关的工作和研究
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