Article(id=1291707091614454263, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.23.007, 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=1785896569397, onlineDateStr=2026-08-05, pubDate=1765900800000, pubDateStr=2025-12-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896569397, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896569397, creator=13701087609, updateTime=1785896569397, updator=13701087609, issue=Issue{id=1291707045514858818, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='23', pageStart='3301', pageEnd='3450', issueExtLink='null', onlineDate='null', pubDate='1765900800000', pubDateStr='2025-12-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896558407, creator='13701087609', updateTime=1785896663780, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707487678390577, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707487682584882, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707045514858818, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3343, endPage=3349, ext={EN=ArticleExt(id=1291707091899666936, articleId=1291707091614454263, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of hyperoside inhibits NF-κB and NLRP3 to promote wound healing in diabetic foot ulcer rats, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the promoting effect and mechanism of hyperoside (Hyp) on wound healing in diabetic foot ulcer (DFU) rats by inhibiting the nuclear factor-kappa B (NF-κB) pathway and the Nod-like receptor family Pyrin domain-containing 3 (NLRP3) inflammasome.
Methods A total of 50 SD rats were randomly divided into blank group, model group, metformin group, low-dose experimental group and high-dose experimental group, with 10 rats in each group. Fasting blood glucose (FBG), wound healing rate and transcutaneous oxygen partial pressure (TcpO2) in the tissues surrounding the wounds were measured using a blood glucose meter. Pathological changes in the wound tissues were observed using hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum levels of interleukin (IL)-8, IL-1β, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP). Western blotting was employed to assess the relative expression levels of matrix metalloproteinase 9 (MMP-9), tissue inhibitor of metalloproteinase 1 (TIMP-1), NF-κB p65, phosphorylated (p)-NF-κB p65 and NLRP3 proteins.
Results The FBG levels in blank, model, metformin, low-dose experimental and high-dose experimental groups were (5.31±0.91), (22.52±3.18), (11.27±2.35), (13.11±2.67) and (8.76±1.15) mmol·L-1, respectively; the wound healing rates were (76.91±12.30)%, (9.53±1.01)%, (45.26±6.15)%, (39.94±5.47)% and (57.10±9.26)%, respectively; the TcpO2 values were (41.09±8.51), (24.35±4.97), (33.27±5.68), (30.84±3.26), and (37.92±4.14) mmHg, respectively; the serum levels of IL-8 were (15.34±0.39), (41.92±3.12), (26.68±2.28), (30.55±3.27) and (17.95±2.70) ng·L-1, respectively; IL-1β levels were (31.05±4.62), (64.39±7.14), (46.62±5.07), (50.21±3.92) and (39.54±4.25) ng·L-1, respectively; TNF-α levels were (26.95±4.15), (69.74±7.43), (39.85±4.29), (45.08±4.36) and (35.52±2.95) ng·L-1, respectively; and CRP levels were (0.69±0.08), (5.11±0.60), (3.23±0.58), (3.68±0.71) and (1.95±0.30) ng·L-1, respectively; the protein relative expression levels of MMP-9 were 0.23±0.03, 0.99±0.11, 0.62±0.05, 0.74±0.06 and 0.39±0.04, respectively; the MMP-9/TIMP-1 ratios were (22.56±1.23)%, (97.07±5.67)%, (60.18±5.01)%, (70.49±5.98)% and (38.39±4.15)%, respectively; the p-NF-κB p65/NF-κB p65 protein relative expression levels were 0.21±0.02, 1.23±0.10, 0.51±0.04, 0.57±0.06 and 0.33±0.04, respectively; and the NLRP3 protein relative expression levels were 0.25±0.01, 0.93±0.07, 0.72±0.08, 0.80±0.06 and 0.35±0.04, respectively. Statistically significant differences were observed when comparing the model group with the blank group and the low- and high-dose experimental groups with the model group (all P<0.05).
Conclusion Hyp promotes wound healing in DFU rats by inhibiting NF-κB and NLRP3 pathways, reducing inflammation and reducing MMP-9 expression.
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目的 探讨金丝桃苷（Hyp）通过抑制核因子κB（NF-κB）通路和Nod样受体家族Pyrin结构域3（NLRP3）炎性小体对糖尿病足溃疡大鼠创面愈合的促进作用及其机制。
方法 将50只SD大鼠按照随机数表法分成空白组、模型组、二甲双胍组、低剂量实验组和高剂量实验组，每组10只。用血糖仪测定各组大鼠的空腹血糖（FBG）、伤口愈合率和创面周围组织经皮氧分压（TcpO2），用苏木精-伊红（HE）染色法观察创面病理组织变化，用酶联免疫吸附实验（ELISA）法检测血清白细胞介素（IL）-8、IL-1β、肿瘤坏死因子α（TNF-α）以及C反应蛋白（CRP）含量，用蛋白质印迹法检测基质金属蛋白酶9（MMP-9）、金属蛋白酶组织抑制因子1（TIMP-1）、NF-κB p65、磷酸化（p）-NF-κB p65和NLRP3蛋白相对表达水平。
结果 干预28天后，空白组、模型组、二甲双胍组和低、高剂量实验组的FBG分别为（5.31±0.91）、（22.52±3.18）、（11.27±2.35）、（13.11±2.67）和（8.76±1.15）mmol·L-1；伤口愈合率分别为（76.91±12.30）%、（9.53±1.01）%、（45.26±6.15）%、（39.94±5.47）%和（57.10±9.26）%；TcpO2分别为（41.09±8.51）、（24.35±4.97）、（33.27±5.68）、（30.84±3.26）和（37.92±4.14）mmHg；IL-8水平为（15.34±0.39）、（41.92±3.12）、（26.68±2.28）、（30.55±3.27）和（17.95±2.70）ng·L-1；IL-1β水平为（31.05±4.62）、（64.39±7.14）、（46.62±5.07）、（50.21±3.92）和（39.54±4.25）ng·L-1；TNF-α水平为（26.95±4.15）、（69.74±7.43）、（39.85±4.29）、（45.08±4.36）和（35.52±2.95）ng·L-1；CRP水平分别为（0.69±0.08）、（5.11±0.60）、（3.23±0.58）、（3.68±0.71）和（1.95±0.30）ng·L-1；MMP-9蛋白相对表达水平分别为0.23±0.03、0.99±0.11、0.62±0.05、0.74±0.06和0.39±0.04；MMP-9/TIMP-1比例分别为（22.56±1.23）%、（97.07±5.67）%、（60.18±5.01）%、（70.49±5.98）%和（38.39±4.15）%；p-NF-κB p65/NF-κB p65蛋白相对表达水平分别为0.21±0.02、1.23±0.10、0.51±0.04、0.57±0.06和0.33±0.04；NLRP3蛋白相对表达水平分别为0.25±0.01、0.93±0.07、0.72±0.08、0.80±0.06和0.35±0.04。模型组的上述指标与空白组比较，低、高剂量实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 Hyp通过抑制NF-κB和NLRP3通路，减轻炎症并降低MMP-9表达，从而促进DFU大鼠创面愈合。
, authors=朱秋霄, 刘子渤, 树林一, 郝志华, 郝慧瑶, authorsList=朱秋霄, 刘子渤, 树林一, 郝志华, 郝慧瑶, authorCompany=null, correspAuthors=郝慧瑶, authorNote=
朱秋霄（1987-），男，主治医师，主要从事糖尿病足、糖尿病周围血管病变相关的临床工作和研究
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