Article(id=1292130335194641382, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130221843571059, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.08.018, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773417600000, receivedDateStr=2026-03-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997478531, onlineDateStr=2026-08-06, pubDate=1777305600000, pubDateStr=2026-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997478531, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997478531, creator=13701087609, updateTime=1785997478531, 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=1164, endPage=1169, ext={EN=ArticleExt(id=1292130335630848999, articleId=1292130335194641382, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of curcumin inhibiting ferroptosis and improving neuronal functional impairment in mice with intracerebral hemorrhage by regulating SPP1, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To investigate the effects of curcumin on ferroptosis and neurological deficit in mice with intracerebral hemorrhage (ICH) and to clarify its potential molecular mechanism.

Methods

A total of 40 mice were divided into sham group, model group, experimental group and inhibitor group, with 10 mice in each group. Intracerebral hemorrhage model in mice was established by tail vein autologous blood injection. The sham group was injected with the same amount of normal saline; in the model group, the model group was established and injected with the same amount of normal saline; the experimental group was intragastrically administered with 200 mg·kg-1 curcumin, and the inhibitor group was intraperitoneally injected with 5 mg·kg-1 secretory phosphoprotein 1 (SPP1) inhibitor solution on the basis of 200 mg·kg-1 curcumin. At the end of the treatment, Longa score was used to evaluate the neurological deficit; the serum levels of Fe2+, malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by enzyme-linked immunosorbent assay (ELISA); the relative fluorescence intensity of reactive oxygen species (ROS) in brain tissue was detected by immunofluorescence method; the relative expression levels of B-cell lymphoma 2 (BCL-2), BCL-2-associated X protein (Bax), nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione peroxidase (GPX4) were detected by Western blot; the relative positive level of SPP1 in brain tissue was detected by immunohistochemistry.

Results

The neurological deficit scores of sham group, model group, experimental group and inhibitor group were (0±0), (3.20±0.42), (1.40±0.52) and (2.10±0.57) scores, respectively; the serum Fe2+levels were (220.35±26.17), (432.40±65.28), (276.52±33.20) and (329.15±45.71) μmol·kg-1, respectively; the serum MDA levels were (53.75±7.62), (120.36±18.22), (72.68±11.23) and (89.44±13.16) nmol·mg-1, respectively; the serum SOD levels were (63.78±9.80), (20.86±3.41), (51.18±7.30) and (37.35±5.08) U·mg-1, respectively; the relative fluorescence intensities of ROS were 1.00±0.09, 3.87±0.56, 1.52±0.22 and 2.43±0.38, respectively; the relative expression levels of Bax in brain tissue were 1.00±0.11, 2.95±0.33, 1.58±0.26 and 2.37±0.29, respectively; the relative expression levels of Bcl-2 were 1.00±0.15, 0.20±0.04, 0.65±0.12 and 0.43±0.07, respectively; the relative expression levels of Nrf2 were 1.00±0.13, 0.33±0.05, 0.65±0.10 and 0.54±0.09, respectively; the relative expression levels of GPX4 were 1.00±0.14, 0.21±0.04, 0.58±0.09 and 0.45±0.06, respectively; the relative positive levels of SPP1 were 1.00±0.13, 0.30±0.05, 0.76±0.12 and 0.43±0.07, respectively. There were statistically significant differences in the above indicators between the model group and the sham operation group, between the experimental group and the model group, and between the inhibitor group and the experimental group (P<0.05, P<0.01, P<0.001).

Conclusion

Curcumin can alleviate neuronal apoptosis and ferroptosis after ICH, and improve neurological function injury in mice. The underlying mechanism may be associated with the up-regulation of SPP1 expression, which in turn activates the Nrf2/GPX4 signaling pathway.

, authors=Xi-xi QU1, Xiu-min ZHAO2a, Jian-lin WANG2b, Hai-bo MA2a, authorsList=Xi-xi QU, Xiu-min ZHAO, Jian-lin WANG, Hai-bo MA, authorCompany=null, correspAuthors=Hai-bo MA, 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=1292130336410989544, articleId=1292130335194641382, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=姜黄素通过调控SPP1抑制脑出血小鼠脑内铁死亡并改善神经功能损伤的研究, 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

探讨姜黄素对脑出血小鼠脑内铁死亡及神经功能损伤的影响,并阐明其潜在分子机制。

方法

将40只小鼠分为假手术组、模型组、实验组及抑制剂组,每组10只。用尾静脉自体血注射法构建小鼠脑出血模型。假手术组注射等量生理盐水,模型组建模并注射等量生理盐水,实验组造模后每日灌胃200 mg·kg-1姜黄素,抑制剂组在200 mg·kg-1姜黄素基础上,每日腹腔注射5 mg·kg-1分泌型磷蛋白1(SPP1)抑制剂溶液。给药结束后,用Longa评分标准进行神经功能缺损评分,用酶联免疫吸附试验(ELISA)法检测血清Fe2+、丙二醛(MDA)及超氧化物歧化酶(SOD)水平;用免疫荧光法检测脑组织活性氧(ROS)相对荧光强度;用蛋白质印迹法检测B细胞淋巴瘤因子2(BCL-2)、BCL-2相关X蛋白(Bax)、核因子红细胞2相关因子2(Nrf2)和谷胱甘肽过氧化物酶4(GPX4)表达水平;用免疫组化法检测脑组织SPP1相对阳性水平。

结果

假手术组、模型组、实验组及抑制剂组的神经功能缺损评分分别为(0±0)、(3.20±0.42)、(1.40±0.52)和(2.10±0.57)分;血清中Fe2+水平分别为(220.35±26.17)、(432.40±65.28)、(276.52±33.20)和(329.15±45.71)μmol·kg-1;血清中MDA水平分别为(53.75±7.62)、(120.36±18.22)、(72.68±11.23)和(89.44±13.16)nmol·mg-1;血清中SOD水平分别为(63.78±9.80)、(20.86±3.41)、(51.18±7.30)和(37.35±5.08)U·mg-1;ROS相对荧光强度分别为1.00±0.09、3.87±0.56、1.52±0.22和2.43±0.38;脑组织中Bax相对表达水平分别为1.00±0.11、2.95±0.33、1.58±0.26和2.37±0.29;BCL-2相对表达水平分别为1.00±0.15、0.20±0.04、0.65±0.12和0.43±0.07;Nrf2相对表达水平分别为1.00±0.13、0.33±0.05、0.65±0.10和0.54±0.09;GPX4相对表达水平分别为1.00±0.14、0.21±0.04、0.58±0.09和0.45±0.06;SPP1相对阳性水平分别为1.00±0.13、0.30±0.05、0.76±0.12和0.43±0.07,模型组与假手术相比、实验组与模型组相比、抑制剂组与实验组相比,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)。

结论

姜黄素能减轻脑出血后神经细胞凋亡与铁死亡,改善小鼠神经功能损伤,其机制可能与上调SPP1表达,进而激活Nrf2/GPX4通路激活有关。

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屈茜茜(1989-),女,主治医师,主要从事心脑血管病方面的研究

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马海波,副主任医师 MP: 13235314212 E-mail:
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姜黄素通过调控SPP1抑制脑出血小鼠脑内铁死亡并改善神经功能损伤的研究
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屈茜茜 1 , 赵修敏 2a , 王建林 2b , 马海波 2a
中国临床药理学杂志 | 临床与基础桥接研究 2026,42(8): 1164-1169
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中国临床药理学杂志 |临床与基础桥接研究 2026 , 42 (8) : 1164 -1169
姜黄素通过调控SPP1抑制脑出血小鼠脑内铁死亡并改善神经功能损伤的研究
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屈茜茜1, 赵修敏2a, 王建林2b, 马海波2a
作者信息
  • 1.济南市中心医院 中医科,山东 济南 250013
  • 2a.山东大学 附属山东省立第三医院 神经内科,山东 济南 250031
  • 2b.山东大学 附属山东省立第三医院 急诊医学科,山东 济南 250031
通讯作者:
马海波,副主任医师 MP: 13235314212 E-mail:
作者简介:

屈茜茜(1989-),女,主治医师,主要从事心脑血管病方面的研究

Research of curcumin inhibiting ferroptosis and improving neuronal functional impairment in mice with intracerebral hemorrhage by regulating SPP1
Xi-xi QU1, Xiu-min ZHAO2a, Jian-lin WANG2b, Hai-bo MA2a
Affiliations
  • 1.Department of Traditional Chinese Medicine, Jinan Central Hospital, Jinan 250013, Shandong Province, China
  • 2a.Department of Neurology; Shandong Provincial Third Hospital Affiliated to Shandong University, Jinan 250031, Shandong Province, China
  • 2b.Department of Emergency Medicine; Shandong Provincial Third Hospital Affiliated to Shandong University, Jinan 250031, Shandong Province, China
出版时间: 2026-04-28 doi: 10.13699/j.cnki.1001-6821.2026.08.018
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目的

探讨姜黄素对脑出血小鼠脑内铁死亡及神经功能损伤的影响,并阐明其潜在分子机制。

方法

将40只小鼠分为假手术组、模型组、实验组及抑制剂组,每组10只。用尾静脉自体血注射法构建小鼠脑出血模型。假手术组注射等量生理盐水,模型组建模并注射等量生理盐水,实验组造模后每日灌胃200 mg·kg-1姜黄素,抑制剂组在200 mg·kg-1姜黄素基础上,每日腹腔注射5 mg·kg-1分泌型磷蛋白1(SPP1)抑制剂溶液。给药结束后,用Longa评分标准进行神经功能缺损评分,用酶联免疫吸附试验(ELISA)法检测血清Fe2+、丙二醛(MDA)及超氧化物歧化酶(SOD)水平;用免疫荧光法检测脑组织活性氧(ROS)相对荧光强度;用蛋白质印迹法检测B细胞淋巴瘤因子2(BCL-2)、BCL-2相关X蛋白(Bax)、核因子红细胞2相关因子2(Nrf2)和谷胱甘肽过氧化物酶4(GPX4)表达水平;用免疫组化法检测脑组织SPP1相对阳性水平。

结果

假手术组、模型组、实验组及抑制剂组的神经功能缺损评分分别为(0±0)、(3.20±0.42)、(1.40±0.52)和(2.10±0.57)分;血清中Fe2+水平分别为(220.35±26.17)、(432.40±65.28)、(276.52±33.20)和(329.15±45.71)μmol·kg-1;血清中MDA水平分别为(53.75±7.62)、(120.36±18.22)、(72.68±11.23)和(89.44±13.16)nmol·mg-1;血清中SOD水平分别为(63.78±9.80)、(20.86±3.41)、(51.18±7.30)和(37.35±5.08)U·mg-1;ROS相对荧光强度分别为1.00±0.09、3.87±0.56、1.52±0.22和2.43±0.38;脑组织中Bax相对表达水平分别为1.00±0.11、2.95±0.33、1.58±0.26和2.37±0.29;BCL-2相对表达水平分别为1.00±0.15、0.20±0.04、0.65±0.12和0.43±0.07;Nrf2相对表达水平分别为1.00±0.13、0.33±0.05、0.65±0.10和0.54±0.09;GPX4相对表达水平分别为1.00±0.14、0.21±0.04、0.58±0.09和0.45±0.06;SPP1相对阳性水平分别为1.00±0.13、0.30±0.05、0.76±0.12和0.43±0.07,模型组与假手术相比、实验组与模型组相比、抑制剂组与实验组相比,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)。

结论

姜黄素能减轻脑出血后神经细胞凋亡与铁死亡,改善小鼠神经功能损伤,其机制可能与上调SPP1表达,进而激活Nrf2/GPX4通路激活有关。

姜黄素  /  脑出血  /  分泌型磷蛋白1  /  核因子红细胞2相关因子2/谷胱甘肽过氧化物酶4通路  /  铁死亡
Objective

To investigate the effects of curcumin on ferroptosis and neurological deficit in mice with intracerebral hemorrhage (ICH) and to clarify its potential molecular mechanism.

Methods

A total of 40 mice were divided into sham group, model group, experimental group and inhibitor group, with 10 mice in each group. Intracerebral hemorrhage model in mice was established by tail vein autologous blood injection. The sham group was injected with the same amount of normal saline; in the model group, the model group was established and injected with the same amount of normal saline; the experimental group was intragastrically administered with 200 mg·kg-1 curcumin, and the inhibitor group was intraperitoneally injected with 5 mg·kg-1 secretory phosphoprotein 1 (SPP1) inhibitor solution on the basis of 200 mg·kg-1 curcumin. At the end of the treatment, Longa score was used to evaluate the neurological deficit; the serum levels of Fe2+, malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by enzyme-linked immunosorbent assay (ELISA); the relative fluorescence intensity of reactive oxygen species (ROS) in brain tissue was detected by immunofluorescence method; the relative expression levels of B-cell lymphoma 2 (BCL-2), BCL-2-associated X protein (Bax), nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione peroxidase (GPX4) were detected by Western blot; the relative positive level of SPP1 in brain tissue was detected by immunohistochemistry.

Results

The neurological deficit scores of sham group, model group, experimental group and inhibitor group were (0±0), (3.20±0.42), (1.40±0.52) and (2.10±0.57) scores, respectively; the serum Fe2+levels were (220.35±26.17), (432.40±65.28), (276.52±33.20) and (329.15±45.71) μmol·kg-1, respectively; the serum MDA levels were (53.75±7.62), (120.36±18.22), (72.68±11.23) and (89.44±13.16) nmol·mg-1, respectively; the serum SOD levels were (63.78±9.80), (20.86±3.41), (51.18±7.30) and (37.35±5.08) U·mg-1, respectively; the relative fluorescence intensities of ROS were 1.00±0.09, 3.87±0.56, 1.52±0.22 and 2.43±0.38, respectively; the relative expression levels of Bax in brain tissue were 1.00±0.11, 2.95±0.33, 1.58±0.26 and 2.37±0.29, respectively; the relative expression levels of Bcl-2 were 1.00±0.15, 0.20±0.04, 0.65±0.12 and 0.43±0.07, respectively; the relative expression levels of Nrf2 were 1.00±0.13, 0.33±0.05, 0.65±0.10 and 0.54±0.09, respectively; the relative expression levels of GPX4 were 1.00±0.14, 0.21±0.04, 0.58±0.09 and 0.45±0.06, respectively; the relative positive levels of SPP1 were 1.00±0.13, 0.30±0.05, 0.76±0.12 and 0.43±0.07, respectively. There were statistically significant differences in the above indicators between the model group and the sham operation group, between the experimental group and the model group, and between the inhibitor group and the experimental group (P<0.05, P<0.01, P<0.001).

Conclusion

Curcumin can alleviate neuronal apoptosis and ferroptosis after ICH, and improve neurological function injury in mice. The underlying mechanism may be associated with the up-regulation of SPP1 expression, which in turn activates the Nrf2/GPX4 signaling pathway.

curcumin  /  intracerebral hemorrhage  /  secreted phosphoprotein 1  /  nuclear factor erythroid 2-related factor 2/glutathione peroxidase signaling pathway  /  ferroptosis
屈茜茜, 赵修敏, 王建林, 马海波. 姜黄素通过调控SPP1抑制脑出血小鼠脑内铁死亡并改善神经功能损伤的研究. 中国临床药理学杂志, 2026 , 42 (8) : 1164 -1169 . DOI: 10.13699/j.cnki.1001-6821.2026.08.018
Xi-xi QU, Xiu-min ZHAO, Jian-lin WANG, Hai-bo MA. Research of curcumin inhibiting ferroptosis and improving neuronal functional impairment in mice with intracerebral hemorrhage by regulating SPP1[J]. Chinese Journal of Clinical Pharmacology, 2026 , 42 (8) : 1164 -1169 . DOI: 10.13699/j.cnki.1001-6821.2026.08.018
  • 山东省医药卫生科技基金资助项目(202303071319)
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doi: 10.13699/j.cnki.1001-6821.2026.08.018
  • 接收时间:2026-03-14
  • 首发时间:2026-08-06
  • 出版时间:2026-04-28
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  • 收稿日期:2026-03-14
基金
山东省医药卫生科技基金资助项目(202303071319)
作者信息
    1.济南市中心医院 中医科,山东 济南 250013
    2a.山东大学 附属山东省立第三医院 神经内科,山东 济南 250031
    2b.山东大学 附属山东省立第三医院 急诊医学科,山东 济南 250031

通讯作者:

马海波,副主任医师 MP: 13235314212 E-mail:
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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