Article(id=1292135423405478672, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.11.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1756742400000, receivedDateStr=2025-09-02, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998691654, onlineDateStr=2026-08-06, pubDate=1781625600000, pubDateStr=2026-06-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998691654, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998691654, creator=13701087609, updateTime=1785998691654, updator=13701087609, issue=Issue{id=1292135402790482407, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='11', pageStart='1501', pageEnd='1650', issueExtLink='null', onlineDate='null', pubDate='1781625600000', pubDateStr='2026-06-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785998686739, creator='13701087609', updateTime=1786014315540, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292200954833686587, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292200954833686588, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1552, endPage=1559, ext={EN=ArticleExt(id=1292135425221612305, articleId=1292135423405478672, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the effect of baicalin on renal injury in nephrotic syndrome rats by regulating the HMGB1/TLR4/NF-κB pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To discuss the effect of baicalin on renal injury in nephrotic syndrome (NS) rats by regulating the high mobility group protein B1 (HMGB1)/Toll like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway.
Methods SD rats were divided into control group, model group, experimental group, HMGB1 inhibitor group and HMGB1 activator group, with 12 rats in each group. Except for the control group, rats in all other groups were injected with adriamycin via the tail vein to establish the nephrotic syndrome (NS) model. Twenty-four hours after successful modeling, the rats in the experimental group were administered 100 mg·kg-1 baicalin by gavage; rats in the HMGB1 inhibitor group were administered 0.03 g·kg-1 HMGB1 inhibitor glycyrrhizic acid by gavage; rats in the HMGB1 activator group were administered 100 mg·kg-1 baicalin by gavage combined with intraperitoneal injection of 8 μg·kg-1 HMGB1 activator recombinant HMGB1 protein (rHMGB1); rats in the model group and control group were administered 10 mL·kg-1 normal saline by gavage and intraperitoneal injection. All treatments were administered once daily for 30 consecutive days. Measure 24-hour urinary protein, serum creatinine, blood urea nitrogen levels, renal pathology, and renal levels of interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α). TUNEL staining was used to detect the apoptosis rate of cells in renal tissue. Western blot was used to detect renal caspase-3, p53, HMGB1, TLR4, and p-NF-κB p65 proteins.
Results In the model group, the renal tissue showed thickening of the glomerular basement membrane, glomerular atrophy, and extensive inflammatory cell infiltration; the 24 h urinary protein levels in the control group, model group, experimental group, HMGB1 inhibitor group, and HMGB1 activator group were (65.56±4.73), (212.19±12.26), (87.76±5.15), (95.53±6.11) and (138.87±8.25) mg·24 h-1, respectively; the serum creatinine levels were (51.57±3.18), (128.86±7.25), (63.69±4.12), (70.75±4.06) and (95.73±5.29) μmol·L-1, respectively; the serum blood urea nitrogen levels were (4.23±0.25), (10.68±0.61), (5.44±0.32), (6.18±0.39) and (8.78±0.53) mmol·L-1, respectively; the renal tissue IL-1β levels were (37.65±2.18), (83.39±5.07), (44.55±2.56), (50.52±2.89) and (69.89±4.17) pg·mL-1, respectively; the renal tissue MCP-1 levels were (156.69±8.12), (314.45±17.36), (181.54±10.21), (201.16±11.54) and (264.45±14.58) pg·mL-1, respectively; the renal tissue TNF-α levels were (34.99±2.15), (90.81±5.63), (43.78±2.52), (51.19±3.15) and (67.11±3.89) pg·mL-1, respectively; the renal tissue apoptosis rates were (4.67±0.31)%, (28.81±1.76)%, (7.08±0.39)%, (8.26±0.51)% and (18.22±1.03)%, respectively; the renal tissue Caspase-3 protein expression levels were 0.86±0.10, 2.37±0.16, 0.98±0.09, 1.21±0.18 and 1.85±0.17, respectively; the renal tissue tumor protein p53 (p53) protein expression levels were 0.15±0.02, 0.68±0.07, 0.24±0.03, 0.36±0.04 and 0.51±0.05, respectively; the renal tissue HMGB1 protein expression levels were 0.65±0.08, 2.04±0.17, 0.87±0.09, 0.95±0.08 and 1.34±0.13, respectively; the renal tissue TLR4 protein expression levels were 0.41±0.05, 1.68±0.16, 0.63±0.07, 0.79±0.08 and 1.09±0.11, respectively; the renal tissue p-NF-κB p65 protein expression levels were 0.23±0.03, 0.81±0.09, 0.37±0.05, 0.45±0.04 and 0.68±0.07, respectively. All differences between the control group and the model group, between the model group and the experimental group/HMGB1 inhibitor group, and between the experimental group and the HMGB1 activator group were all statistically significant (all P<0.05).
Conclusion Baicalin may inhibit the inflammatory response and cell apoptosis in NS rats, and alleviate renal injury by suppressing HMGB1/TLR4/NF-κB pathway.
, authors=Pu GONG
1a, Qing WANG
1b, authorsList=Pu GONG, Qing WANG, authorCompany=null, correspAuthors=Qing 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=1292135425561350930, articleId=1292135423405478672, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=黄芩苷调控HMGB1/TLR4/NF-κB通路对肾病综合征大鼠肾损伤影响的研究, 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 探讨黄芩苷调控高迁移率族蛋白B1（HMGB1）/Toll样受体4（TLR4）/核因子κB（NF-κB）通路对肾病综合征（NS）大鼠肾损伤的影响。
方法 SD大鼠分为对照组、模型组、实验组、HMGB1抑制剂组和HMGB1激活剂组，每组12只。除对照组外，其他组大鼠均通过尾静脉注射阿霉素的方式构建NS模型，建模成功24 h后处理，实验组大鼠灌胃100 mg·kg-1黄芩苷；HMGB1抑制剂组大鼠灌胃0.03 g·kg-1 HMGB1抑制剂甘草酸；HMGB1激活剂组大鼠灌胃100 mg·kg-1黄芩苷且腹腔注射8 μg·kg-1 HMGB1激活剂HMGB1重组蛋白（rHMGB1）；模型组和对照组大鼠灌胃且腹腔注射10 mL·kg-1生理盐水。每天处理1次，持续30 d。检测24 h尿蛋白、血清血肌酐、尿素氮水平、肾脏病理及肾脏白细胞介素-1β（IL-1β）、单核细胞趋化蛋白- 1（MCP-1）、肿瘤坏死因子- α（TNF-α）水平；用TUNEL染色法检测肾脏组织中细胞凋亡率；用蛋白质印迹法检测肾脏半胱氨酸天冬氨酸蛋白酶3（Caspase-3）、肿瘤蛋白p53（p53）、HMGB1、TLR4、p-NF-κB p65蛋白相对表达水平。
结果 模型组大鼠肾脏组织中肾小球基底膜增厚，肾小球萎缩，有大量炎性细胞浸润。对照组、模型组、实验组、HMGB1抑制剂组和HMGB1激活剂组大鼠24 h尿蛋白分别为（65.56±4.73）、（212.19±12.26）、（87.76±5.15）、（95.53±6.11）和（138.87±8.25）mg·24 h-1；血清血肌酐分别为（51.57±3.18）、（128.86±7.25）、（63.69±4.12）、（70.75±4.06）和（95.73±5.29）μmol·L-1；血清尿素氮分别为（4.23±0.25）、（10.68±0.61）、（5.44±0.32）、（6.18±0.39）和（8.78±0.53）mmol·L-1；肾脏组织IL-1β水平分别为（37.65±2.18）、（83.39±5.07）、（44.55±2.56）、（50.52±2.89）和（69.89±4.17）pg·mL-1；肾脏组织MCP-1水平分别为（156.69±8.12）、（314.45±17.36）、（181.54±10.21）、（201.16±11.54）和（264.45±14.58）pg·mL-1；肾脏组织TNF-α水平分别为（34.99±2.15）、（90.81±5.63）、（43.78±2.52）、（51.19±3.15）和（67.11±3.89）pg·mL-1；肾脏组织细胞凋亡率分别为（4.67±0.31）%、（28.81±1.76）%、（7.08±0.39）%、（8.26±0.51）%和（18.22±1.03）%；肾脏组织Caspase-3蛋白相对表达水平分别为0.86±0.10、2.37±0.16、0.98±0.09、1.21±0.18和1.85±0.17；肾脏组织p53蛋白相对表达水平分别为0.15±0.02、0.68±0.07、0.24±0.03、0.36±0.04和0.51±0.05；肾脏组织HMGB1蛋白相对表达水平分别为0.65±0.08、2.04±0.17、0.87±0.09、0.95±0.08和1.34±0.13；肾脏组织TLR4蛋白相对表达水平分别为0.41±0.05、1.68±0.16、0.63±0.07、0.79±0.08和1.09±0.11；肾脏组织p-NF-κB p65蛋白相对表达水平分别为0.23±0.03、0.81±0.09、0.37±0.05、0.45±0.04和0.68±0.07，对照组的上述指标与模型组比较，模型组与实验组、HMGB1抑制剂组比较，实验组与HMGB1激活剂组比较，在统计学上差异有统计学意义（均P<0.05）。
结论 黄芩苷可能通过下调HMGB1/TLR4/NF-κB抑制NS大鼠炎症及细胞凋亡，减轻肾损伤。
, authors=宫璞
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宫璞（1988-），女，主治医师，从事肾病的中西医结合临床工作和研究
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