Article(id=1292130242299191784, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.08.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773590400000, receivedDateStr=2026-03-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997456382, onlineDateStr=2026-08-06, pubDate=1777305600000, pubDateStr=2026-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997456382, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997456382, creator=13701087609, updateTime=1785997456382, updator=13701087609, issue=Issue{id=1292130221843571059, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1777305600000', pubDateStr='2026-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997451505, creator='13701087609', updateTime=1786014411018, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201355276480844, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201355276480845, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1130, endPage=1136, ext={EN=ArticleExt(id=1292130244119519721, articleId=1292130242299191784, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of rosmarinic acid inhibiting macrophage M1 polarization and alleviating lipopolysaccharide-induced acute kidney injury, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the potential mechanism of rosmarinic acid in reducing sepsis related kidney injury.
Methods In the animal experiment, BALB/c mice were randomly divided into animal control group, animal model group [10 mg·kg-1 lipopolysaccharide (LPS) modeling], animal low-dose experimental group (modeling+10 mg·kg-1 rosmarinic acid) and animal high-dose experimental group (modeling+20 mg·kg-1 rosmarinic acid), with 10 mice in each group. In the cell experiment part, RAW264.7 cells were randomly divided into cell blank group, cell model group (1 μg·mL-1 LPS), cell low-dose experimental group (modeling+20.00 μmol·mL-1 rosmarinic acid) and cell high-dose experimental group (modeling+40.00 μmol·mL-1 rosmarinic acid). Serum and renal tissue inflammatory related indicators were analyzed by enzyme linked immunosorbent assay (ELISA) kit and real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). Renal tissue differentiation cluster 86 (CD86)+cells and F4/80+cells were co-located by immunohistochemistry.
Results In the animal experiment part, the serum creatinine (Scr) levels of animal control group, animal model group, low-dose experimental group and high-dose experimental group were (14.80±0.73), (59.73±6.79), (50.06±5.12) and (43.62±3.73) mmol·L-1, respectively; the levels of inducible nitric oxide synthase (iNOS) were (1.26±0.11), (4.74±0.11), (3.86±0.23) and (2.48±0.28) U·L-1, respectively; the levels of tumor necrosis factor-alpha (TNF-α) were (14.00±1.47), (85.90±6.66), (64.97±5.62) and (46.84±1.95) pg·mL-1, respectively; the levels of interleukin (IL)-6 were (6.93±0.47), (50.05±3.84), (39.93±3.50) and (27.26±2.09) pg·mL-1, respectively; the levels of IL-1 β were (22.17±2.27), (122.42±12.77), (91.54±6.84) and (61.23±6.31) pg·mL-1, respectively; the CD86+/F4/80+ co-located cells were (100.00±4.85)%, (476.99±39.89)%, (322.15±24.15)% and (219.90±19.81)%, respectively. There were statistically significant differences in the above indexes between animal model and animal control group, between low-dose, high-dose experimental groups and animal model group, and between high-dose experimental group and low-dose experimental group (P<0.05, P<0.01, P<0.001). In the cell experiment, the relative expression levels of iNOS mRNA in the cell blank group, cell model group, cell low-dose experimental group and cell high-dose experimental group were 1.00±0.10, 3.26±0.31, 2.51±0.27 and 1.94±0.19, respectively; the relative expression levels of TNF - α mRNA were 1.00±0.14, 2.54±0.26, 2.07±0.22 and 1.77±0.18, respectively; the relative expression levels of IL-1β mRNA were 1.00±0.12, 2.24±0.30, 1.83±0.22 and 1.52±0.17, respectively; the relative expression levels of IL-6 mRNA were 1.00±0.08, 2.43±0.17, 1.85±0.21 and 1.54±0.16, respectively. There were statistically significant differences in the above indexes between cell model group and cell blank group, between low-dose and high-dose experimental groups and cell model group, and between high-dose experimental group and low-dose experimental group (P<0.01, P<0.001).
Conclusion Rosmarinic acid plays a protective role in LPS-induced acute kidney injury by inhibit macrophage activation and inhibition of their transformation into M1-type macrophages.
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目的 探讨迷迭香酸减轻脓毒症相关肾损伤的潜在作用机制。
方法 在动物实验部分，将BALB/c小鼠随机分为动物对照组、动物模型组[10 mg·kg-1脂多糖（LPS）建模]、动物低剂量实验组（建模+10 mg·kg-1迷迭香酸）、动物高剂量实验组（建模+20 mg·kg-1迷迭香酸），每组10只。在细胞实验部分，将RAW264.7细胞随机分为细胞空白组、细胞模型组（1 μg·mL-1 LPS）、细胞低剂量实验组（建模+20.00 μmol·mL-1迷迭香酸）和细胞高剂量实验组（建模+40.00 μmol·mL-1迷迭香酸）。用酶联免疫吸附测定（ELISA）试剂盒法及实时荧光定量聚合酶链反应（RT-qPCR）法分析血清及肾组织炎性相关指标，用免疫组织荧光法检测肾组织分化簇86（CD86）+细胞与F4/80+细胞共定位。
结果 在动物实验部分，动物对照组、动物模型组、动物低剂量实验组和动物高剂量实验组的血清肌酸酐（Scr）水平分别为（14.80±0.73）、（59.73±6.79）、（50.06±5.12）和（43.62±3.73）mmol·L-1，诱导型一氧化氮合酶（iNOS）水平分别为（1.26±0.11）、（4.74±0.11）、（3.86±0.23）和（2.48±0.28）U·L-1，肿瘤坏死因子（TNF-α）水平分别为（14.00±1.47）、（85.90±6.66）、（64.97±5.62）和（46.84±1.95）pg·mL-1，白细胞介素（IL）-6水平分别为（6.93±0.47）、（50.05±3.84）、（39.93±3.50）和（27.26±2.09）pg·mL-1，IL-1β水平分别为（22.17±2.27）、（122.42±12.77）、（91.54±6.84）和（61.23±6.31）pg·mL-1；CD86+/F4/80+共定位细胞分别为（100.00±4.85）%、（476.99±39.89）%、（322.15±24.15）%和（219.90±19.81）%，动物模型的与动物对照组比较、动物低、高剂量实验组与动物模型组比较、动物高剂量实验组与动物低剂量实验组比较，上述指标在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。在细胞实验部分，细胞空白组、细胞模型组、细胞低剂量实验组和细胞高剂量实验组的iNOS mRNA相对表达水平分别为1.00±0.10、3.26±0.31、2.51±0.27和1.94±0.19，TNF-α mRNA相对表达水平分别为1.00±0.14、2.54±0.26、2.07±0.22和1.77±0.18，IL-1β mRNA相对表达水平分别为1.00±0.12、2.24±0.30、1.83±0.22和1.52±0.17，IL-6 mRNA相对表达水平分别为1.00±0.08、2.43±0.17、1.85±0.21和1.54±0.16，细胞模型组与细胞空白组比较、细胞低、高剂量实验组与细胞模型组比较、细胞高剂量实验组与细胞低剂量实验组比较，上述指标在统计学上差异均有统计学意义（P<0.01，P<0.001）。
结论 迷迭香酸可以通过抑制巨噬细胞活化并同时抑制其向M1型巨噬细胞转化对LPS诱导的急性肾损伤发挥保护作用。
, authors=何晓华, 徐旭, authorsList=何晓华, 徐旭, authorCompany=null, correspAuthors=徐旭, authorNote=
何晓华（1982-），女，副主任药师，主要从事中药学方面的研究和工作
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