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Article(id=1259888462128362332, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, articleNumber=null, orderNo=null, doi=10.13343/j.cnki.wsxb.20250698, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1757606400000, receivedDateStr=2025-09-12, revisedDate=null, revisedDateStr=null, acceptedDate=1766851200000, acceptedDateStr=2025-12-28, onlineDate=1778310416966, onlineDateStr=2026-05-09, pubDate=1777824000000, pubDateStr=2026-05-04, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1778310416966, onlineIssueDateStr=2026-05-09, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1778310416966, creator=13701087609, updateTime=1778310416966, updator=13701087609, issue=Issue{id=1259888457367806489, tenantId=1146029695717560320, journalId=1192105938417971205, year='2026', volume='66', issue='5', pageStart='2031', pageEnd='2556', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=0, articleOrder=1, issueType=-1, specialIssue=null, createTime=1778310415832, creator=13701087609, updateTime=1778320153326, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1259929299465921482, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1259929299465921483, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=2416, endPage=2429, ext={EN=ArticleExt(id=1259888465152455527, articleId=1259888462128362332, tenantId=1146029695717560320, journalId=1192105938417971205, language=EN, title=Curcumin ameliorates spinal cord injury by regulating the Treg/Th17 balance via gut microbiota, columnId=1192149543992045670, journalTitle=Acta Microbiologica Sinica, columnName=Research Article, runingTitle=null, highlight=null, articleAbstract=

Objective The immunoinflammatory response induced by spinal cord injury is a key factor hindering the recovery of neurological functions. Recent studies have shown that gut microbiota dysbiosis can participate in the immune regulation of the central nervous system through the gut-spinal cord axis. This study aims to explore whether curcumin can exert its protective effect on spinal cord injury by reshaping the gut microbiota and thereby regulating the local Treg/Th17 balance in the spinal cord. Methods Female Sprague-Dawley rats weighing 200‒220 g were randomly assigned into the sham operation group, spinal cord injury group, curcumin group, fecal microbiota transplantation group, fecal microbiota transplantation+ curcumin group, and fecal microbiota transplantation+curcumin+GPR inhibitor group. Neurological function recovery was evaluated based on the Basso-Beattie-Bresnahan motor function score and gait analysis. Histopathological changes in the injured area were observed via hematoxylin-eosin staining, Nissl staining, and Luxol Fast Blue staining. RT-qPCR, ELISA, and Western blotting were employed to quantify the expression levels of key transcription factor forkhead box protein 3 (FOXP3) for Treg cells, anti-inflammatory cytokines interleukin (IL)-10 and transforming growth factor (TGF)-β1, as well as key transcription factor retinoic acid receptor-related orphan receptor gamma t (RORγt) for Th17 cells and pro-inflammatory cytokines IL-17 and IL-6 in the spinal cord of each group. Results Compared with the spinal cord injury group and fecal microbiota transplantation group, the curcumin group and fecal microbiota transplantation+ curcumin group showed the most significant improvement in neurological function, specifically manifested by significant increases in BBB motor function scores and gait coordination, along with a marked reduction in the scope of spinal cord injury. At the molecular level, the two groups showed significantly upregulated gene and protein levels of FOXP3, IL-10, and TGF-β1 and significantly inhibited expression of RORγt, IL-17A, and IL-6 in the spinal cord tissue. This suggests that after curcumin intervention in the gut microbiota, the immune balance shifted toward a Treg-dominated anti-inflammatory state. Notably, the aforementioned beneficial effects of curcumin-modified gut microbiota were reversed after combined use of the GPR inhibitor. Conclusion This study indicates that curcumin can act on the gut microbiota to promote the recovery of motor function after spinal cord injury. Curcumin may exert the effect by activating the GPR signaling pathway, thereby upregulating Treg viability, inhibiting Th17 differentiation, and ultimately correcting the Treg/Th17 imbalance. This provides new experimental evidence and application value for using curcumin and its modified gut microbiota as an adjuvant therapeutic strategy for spinal cord injury.

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E-mail: CHANG Xiaowei, ;
YANG Yanling,
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目的 脊髓损伤后引发的免疫炎症反应是阻碍神经功能恢复的关键因素。近期研究表明，肠道菌群紊乱可通过“肠-脊髓轴”参与中枢神经系统的免疫调控。本研究旨在探讨姜黄素能否通过重塑肠道菌群，调节脊髓局部Treg/Th17平衡，从而发挥对脊髓损伤的保护作用。 方法 将200-220 g左右的雌性Sprague-Dawley (SD)大鼠随机分为假手术组、脊髓损伤组、姜黄素组、粪菌移植组、粪菌移植姜黄素组、粪菌移植姜黄素+GPRs抑制剂组。通过Basso-Beattie-Bresnahan (BBB)运动功能评分和步态分析评估神经功能恢复情况；采用苏木精-伊红染色、尼氏染色和劳克坚牢蓝染色观察损伤区域的组织病理学变化；运用实时荧光定量逆转录PCR检测、酶联免疫吸附测定和蛋白印迹分析，检测各组脊髓中Treg细胞关键转录因子FOXP3、抗炎因子IL-10和TGF-β1，以及Th17细胞关键转录因子RORγt、促炎因子IL-17和IL-6的表达情况。 结果 与脊髓损伤组和粪菌移植组相比，姜黄素组和粪菌移植姜黄素组大鼠的神经功能改善最为显著，具体表现为BBB运动功能评分和步态协调性显著提升，同时脊髓组织损伤范围明显缩小。在分子水平上，这2组脊髓组织中FOXP3、IL-10和TGF-β1的基因和蛋白表达显著上调，而RORγt、IL-17A和IL-6的表达则被显著抑制，这提示姜黄素干预肠道菌群后免疫平衡向Treg主导的抗炎状态倾斜。值得注意的是，联合使用GPRs抑制剂后，姜黄素修饰菌群带来的上述有益效应被逆转。 结论 本研究表明，姜黄素干预后的肠道菌群能够有效促进脊髓损伤后的运动功能恢复，其作用机制可能与激活GPRs信号通路，上调Treg细胞活性、抑制Th17细胞分化，最终纠正Treg/Th17免疫失衡密切相关。这为将姜黄素及其修饰后的肠道菌群作为脊髓损伤的辅助治疗策略提供了新的实验依据和应用价值。

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作者贡献声明

田春平：数据收集与监管，撰写文章；吴佳俊：验证，软件程序，数据分析；肖林峰：执行调研，验证；王青燕：执行调研，方法论；杜嘉妮：执行调研，监督管理；胡倩倩：监督管理；强京灵：方法论；常小卫：提供资源，项目管理，获取基金；杨彦玲：提出概念，提供资源，项目管理，获取基金。

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Biomaterials Advances, 2022, 133: 112624., articleTitle=Spinal cord injury target-immunotherapy with TNF-α autoregulated and feedback-controlled human umbilical cord mesenchymal stem cell derived exosomes remodelled by CRISPR/Cas9 plasmid, refAbstract=null)], funds=[Fund(id=1259928513981854675, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=82560280, language=EN, fundingSource=The National Natural Science Foundation of China(82560280), fundOrder=null, country=null), Fund(id=1259928514799743970, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=82560280, language=CN, fundingSource=国家自然科学基金(82560280), fundOrder=null, country=null), Fund(id=1259928515542135782, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=82560366, language=EN, fundingSource=The National Natural Science Foundation of China(82560366), fundOrder=null, country=null), Fund(id=1259928516066423790, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=82560366, language=CN, fundingSource=国家自然科学基金(82560366), fundOrder=null, country=null), Fund(id=1259928518893384699, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=2024SF-YBXM-037, language=EN, fundingSource=The General Project of Shaanxi Provincial Department of Science and Technology(2024SF-YBXM-037), fundOrder=null, country=null), Fund(id=1259928519421865986, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=2024SF-YBXM-037, language=CN, fundingSource=陕西省科学技术厅一般项目(2024SF-YBXM-037), fundOrder=null, country=null), Fund(id=1259928521091198986, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=2024SLZDCY-021, language=EN, fundingSource=The Project of Yan’an Science and Technology Bureau(2024SLZDCY-021), fundOrder=null, country=null), Fund(id=1259928523549061140, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=2024SLZDCY-021, language=CN, fundingSource=延安市科学技术局项目(2024SLZDCY-021), fundOrder=null, country=null), Fund(id=1259928524425670686, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=YCX2024102, language=EN, fundingSource=The Graduate Education Innovation Program of Yan’an University(YCX2024102), fundOrder=null, country=null), Fund(id=1259928525579104293, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, awardId=YCX2024102, language=CN, fundingSource=延安大学教育创新计划(YCX2024102), fundOrder=null, country=null)], companyList=[AuthorCompany(id=1259928400299438386, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, xref=1., ext=[AuthorCompanyExt(id=1259928400618205491, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, companyId=1259928400299438386, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=1.Yan’an Medical College, Yan’an University, Yan’an, Shaanxi, China), AuthorCompanyExt(id=1259928400643371316, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, companyId=1259928400299438386, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=1.延安大学延安医学院，陕西 延安)]), AuthorCompany(id=1259928401985548609, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, xref=2., ext=[AuthorCompanyExt(id=1259928402279149892, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, companyId=1259928401985548609, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=2.Neurosurgery Department, Yan’an University Affiliated Hospital, Yan’an, Shaanxi, China), AuthorCompanyExt(id=1259928402346258757, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, companyId=1259928401985548609, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=2.延安大学附属医院神经外科，陕西 延安)])], figs=[ArticleFig(id=1259928490359534401, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 1, caption=Expression patterns of Treg and Th17 cells in three rat models. In normal rats, CD4⁺ T cells can differentiate into Treg cells by inducing FOXP3 transcription, leading to the secretion of anti-inflammatory cytokines such as IL-10 and TGF-β1. Alternatively, CD4⁺ T cells can differentiate into Th17 cells by inducing RORγt transcription, promoting the secretion of pro-inflammatory cytokines including IL-6 and IL-17A, thereby maintaining a dynamic balance between Treg and Th17 cells. After SCI, Th17 cell function becomes overactivated, Treg cell function is impaired, and the Treg/Th17 balance is disrupted, resulting in increased pro-inflammatory cytokines. FMT following curcumin intervention restores this balance in SCI rats, reducing inflammation and promoting immune homeostasis., figureFileSmall=qDKMyBfyURxp2u8LzXLEgg==, figureFileBig=PiAyiuUHbAlFnJog2LZA1Q==, tableContent=null), ArticleFig(id=1259928492712538949, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图1, caption=Treg/Th17在3种大鼠模型体内的表达, figureFileSmall=qDKMyBfyURxp2u8LzXLEgg==, figureFileBig=PiAyiuUHbAlFnJog2LZA1Q==, tableContent=null), ArticleFig(id=1259928496424498009, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 2, caption=Grouping of animals in the experiment. This experiment consists of two parts. In the first part, 16 rats are divided into a control group and a curcumin group, with 8 rats in each group. The control group has free access to drinking water, while the experimental group is given intragastric administration of curcumin at a dose of 100 mg/kg per day, and feces of the two groups are collected after 14 days. In the second part, 30 rats are divided into 6 groups, with 5 rats in each group: The Sham group only has the lamina removed without spinal cord contusion; The SCI group receives no drug intervention; The CUR group is directly given intragastric administration of curcumin; The FMT group is given intragastric administration of gut microbiota from normal feces; The FMT+CUR group is given intragastric administration of gut microbiota from curcumin-intervened feces; The FMT+CUR+GLPG0974 group is given intragastric administration of gut microbiota from curcumin-intervened feces and GLPG0974., figureFileSmall=ANjRNNfnIiHPfg0LK60Dww==, figureFileBig=/xW6iI+AWT+6skkNYk8NKg==, tableContent=null), ArticleFig(id=1259928496999117666, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图2, caption=动物实验分组, figureFileSmall=ANjRNNfnIiHPfg0LK60Dww==, figureFileBig=/xW6iI+AWT+6skkNYk8NKg==, tableContent=null), ArticleFig(id=1259928498060276592, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 3, caption=Therapeutic effects of curcumin-modulated FMT in a SCI rat model. A: BBB scores of rats in each group at different time points [*P<0.05, **P<0.01, SCI group vs. FMT group; ns: No significant difference; #P<0.05, ##P<0.01, ###P<0.001, SCI group vs. CUR group; ^P<0.05, ^^P<0.01, ^^^P<0.01, SCI group vs. FMT+CUR group (mean±SD, n=5)]; B: Representative footprint analysis of rats at 28 days after SCI [Blue: Forepaw prints; Red: Hindpaw prints (mean±SD, n=5)]; C: Qualitative analysis of hindpaw footprint length [(mean±SD, n=5); *P<0.05, **P<0.01, ***P<0.001, SCI group vs. other groups]; D: Hematoxylin-eosin (HE) staining, Nissl staining, and Luxol fast blue (LFB) staining of spinal cord sections at 28 days after SCI; E: Statistical analysis of HE staining [(mean±SD, n=5); **P<0.01, ***P<0.001, ****P<0.000 1, Sham group vs. other groups]; F: Statistical analysis of Nissl staining [(mean±SD, n=5); *P<0.05, **P<0.01, ***P<0.001, SCI group vs. other groups]; G: Statistical analysis of LFB staining [(mean±SD, n=5); *P<0.05, **P<0.01, ***P<0.001, SCI group vs. other groups]., figureFileSmall=XeJgG01247XImip5+EJk+g==, figureFileBig=tLngA9hMByJQXOuC5A7KFg==, tableContent=null), ArticleFig(id=1259928499285013371, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图3, caption=姜黄素粪菌移植在脊髓损伤模型中的疗效, figureFileSmall=XeJgG01247XImip5+EJk+g==, figureFileBig=tLngA9hMByJQXOuC5A7KFg==, tableContent=null), ArticleFig(id=1259928501281502085, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 4, caption=Effects of curcumin-modulated FMT on Treg and Th17 cell-associated markers in spinal cord tissues. A: Statistical chart of the RNA-level expression of FOXP3, a transcription factor related to Treg cells, in rat spinal cord tissues detected by RT-qPCR; B: Statistical chart of the RNA-level expression of IL-10, an inflammatory factor related to Treg cells, in rat spinal cord tissues detected by RT-qPCR; C: Statistical chart of the RNA-level expression of TGF-β1, an inflammatory factor related to Treg cells, in rat spinal cord tissues detected by RT-qPCR; D: Statistical chart of the RNA-level expression of RORγt, a transcription factor related to Th17 cells, in rat spinal cord tissues detected by RT-qPCR; E: Statistical chart of the RNA-level expression of IL-17A, an inflammatory factor related to Th17 cells, in rat spinal cord tissues detected by RT-qPCR; F: Statistical chart of the RNA-level expression of IL-6, an inflammatory factor related to Th17 cells, in rat spinal cord tissues detected by RT-qPCR; G: Statistical chart of the protein-level expression of IL-10 in rat spinal cord tissue homogenates detected by ELISA; H: Statistical chart of the protein-level expression of IL-17A in rat spinal cord tissue homogenates detected by ELISA; I: Statistical chart of the protein-level expression of IL-6 in rat spinal cord tissue homogenates detected by ELISA; J: Analysis of the changes in protein expression levels of TGF-β1, FOXP3 and RORγt in rat spinal cord tissues detected by Western blotting; K: Statistical analysis chart of the protein-level expression of RORγt in rat spinal cord tissues; L: Statistical analysis chart of the protein-level expression of FOXP3 in rat spinal cord tissues; M: Statistical analysis chart of the protein-level expression of TGF-β1 in rat spinal cord tissues. All data are presented as mean±SD (n=3). *P<0.05, **P<0.01, ***P<0.001 in other groups vs. SCI group., figureFileSmall=tc4i6r/n1zpdurtT8Df/3g==, figureFileBig=mv4PMQS1HUD85LuKTHSnFA==, tableContent=null), ArticleFig(id=1259928503898747794, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图4, caption=姜黄素粪菌移植对Treg和Th17细胞的影响, figureFileSmall=tc4i6r/n1zpdurtT8Df/3g==, figureFileBig=mv4PMQS1HUD85LuKTHSnFA==, tableContent=null), ArticleFig(id=1259928505140261786, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 5, caption=Original Western blotting images. A: Original RORγt image corresponding to Figure 4J; B: Original FOXP3 image corresponding to Figure 4J; C: Original TGF-β1 image corresponding to Figure 4J; D: Original RORγt image corresponding to Figure 6B; E: Original FOXP3 image corresponding to Figure 6B; F: Original TGF-β1 image corresponding to Figure 6B., figureFileSmall=ZGNlbKcO8rev23sqstolHA==, figureFileBig=b+6v45kua0BAlFfGnDuZ8g==, tableContent=null), ArticleFig(id=1259928506327249826, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图5, caption=Western blotting原图, figureFileSmall=ZGNlbKcO8rev23sqstolHA==, figureFileBig=b+6v45kua0BAlFfGnDuZ8g==, tableContent=null), ArticleFig(id=1259928507249996711, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Figure 6, caption=Curcumin regulates Treg/Th17 cell differentiation via modulation of the gut microbiota. A: Statistical graphs of the protein expression levels of IL-10, IL-17A, and IL-6 in rat spinal cord tissue homogenates detected by ELISA; B: Analysis of the changes in protein expression levels of TGF-β1, FOXP3, and RORγt in rat spinal cord tissues; C: Statistical analysis chart of the protein-levels expression of RORγt, FOXP3, and TGF-β1 in rat spinal cord tissues. All data are presented as mean±SD (n=3). *P<0.05, **P<0.01, ***P<0.001 in other groups vs. SCI group., figureFileSmall=8K8DpAkwYtshqFs0ZqmZ2w==, figureFileBig=ZOje+ulpp9G1G4r5D4CTLQ==, tableContent=null), ArticleFig(id=1259928510072763315, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=图6, caption=姜黄素通过肠道菌群调节Treg/Th17细胞分化, figureFileSmall=8K8DpAkwYtshqFs0ZqmZ2w==, figureFileBig=ZOje+ulpp9G1G4r5D4CTLQ==, tableContent=null), ArticleFig(id=1259928510911624125, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=EN, label=Table 1, caption=

Primers used in this study

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)Accession No.Product length/bp
β-actin

F: CACTATCGGCAATGAGCGGTTC

R: CAGCACTGTGTTGGCATAGAGG

NM_031144.3154
FOXP3

F: AGAGAGGCAGAGGACACTCAATG

R: GGTTGTGGCGGATGGCATTC

NM_001108250.2104
IL-10

F: CCCTGGGAGAGAAGCTGAAGAC

R: TCACCTGCTCCACTGCCTTG

NM_012854.296
TGF-β1

F: GACCGCAACAACGCAATCTATGAC

R: CTGGCACTGCTTCCCGAATGTC

NM_021578.294
RORγt

F: ACCACCCTCTTCTCACGGG

R: CTTCCATTGCTCCTGCTTTC

XM_017591313.3190
IL-17A

F: CCTGATGCTGTTGCTGCTACTG

R: GCGTTTGGACACACTGAACTTTG

NM_001106897.184
IL-6

F: GTTTCTCTCCGCAAGAGACTTC

R: TCTCCTCTCCGGACTTGTGAA

NM_012589.296
), ArticleFig(id=1259928511347831748, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888462128362332, language=CN, label=表1, caption=

本研究所用引物

, figureFileSmall=null, figureFileBig=null, tableContent=
Primer namesPrimer sequences (5′→3′)Accession No.Product length/bp
β-actin

F: CACTATCGGCAATGAGCGGTTC

R: CAGCACTGTGTTGGCATAGAGG

NM_031144.3154
FOXP3

F: AGAGAGGCAGAGGACACTCAATG

R: GGTTGTGGCGGATGGCATTC

NM_001108250.2104
IL-10

F: CCCTGGGAGAGAAGCTGAAGAC

R: TCACCTGCTCCACTGCCTTG

NM_012854.296
TGF-β1

F: GACCGCAACAACGCAATCTATGAC

R: CTGGCACTGCTTCCCGAATGTC

NM_021578.294
RORγt

F: ACCACCCTCTTCTCACGGG

R: CTTCCATTGCTCCTGCTTTC

XM_017591313.3190
IL-17A

F: CCTGATGCTGTTGCTGCTACTG

R: GCGTTTGGACACACTGAACTTTG

NM_001106897.184
IL-6

F: GTTTCTCTCCGCAAGAGACTTC

R: TCTCCTCTCCGGACTTGTGAA

NM_012589.296
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姜黄素通过肠道菌群调节Treg/Th17平衡改善脊髓损伤
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田春平 1 , 吴佳俊 1 , 肖林峰 1 , 王青燕 1 , 杜嘉妮 1 , 胡倩倩 1 , 强京灵 2 , 常小卫 1 , 杨彦玲 1
微生物学报 | 研究报告 2026,66(5): 2416-2429
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微生物学报 | 研究报告 2026, 66(5): 2416-2429
姜黄素通过肠道菌群调节Treg/Th17平衡改善脊髓损伤
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田春平1, 吴佳俊1, 肖林峰1, 王青燕1, 杜嘉妮1, 胡倩倩1, 强京灵2, 常小卫1 , 杨彦玲1
作者信息
  • 1.延安大学延安医学院，陕西 延安
  • 2.延安大学附属医院神经外科，陕西 延安
Curcumin ameliorates spinal cord injury by regulating the Treg/Th17 balance via gut microbiota
Chunping TIAN1, Jiajun WU1, Linfeng XIAO1, Qingyan WANG1, Jiani DU1, Qianqian HU1, Jingling QIANG2, Xiaowei CHANG1 , Yanling YANG1
Affiliations
  • 1.Yan’an Medical College, Yan’an University, Yan’an, Shaanxi, China
  • 2.Neurosurgery Department, Yan’an University Affiliated Hospital, Yan’an, Shaanxi, China
出版时间: 2026-05-04 doi: 10.13343/j.cnki.wsxb.20250698
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目的 脊髓损伤后引发的免疫炎症反应是阻碍神经功能恢复的关键因素。近期研究表明，肠道菌群紊乱可通过“肠-脊髓轴”参与中枢神经系统的免疫调控。本研究旨在探讨姜黄素能否通过重塑肠道菌群，调节脊髓局部Treg/Th17平衡，从而发挥对脊髓损伤的保护作用。 方法 将200-220 g左右的雌性Sprague-Dawley (SD)大鼠随机分为假手术组、脊髓损伤组、姜黄素组、粪菌移植组、粪菌移植姜黄素组、粪菌移植姜黄素+GPRs抑制剂组。通过Basso-Beattie-Bresnahan (BBB)运动功能评分和步态分析评估神经功能恢复情况；采用苏木精-伊红染色、尼氏染色和劳克坚牢蓝染色观察损伤区域的组织病理学变化；运用实时荧光定量逆转录PCR检测、酶联免疫吸附测定和蛋白印迹分析，检测各组脊髓中Treg细胞关键转录因子FOXP3、抗炎因子IL-10和TGF-β1，以及Th17细胞关键转录因子RORγt、促炎因子IL-17和IL-6的表达情况。 结果 与脊髓损伤组和粪菌移植组相比，姜黄素组和粪菌移植姜黄素组大鼠的神经功能改善最为显著，具体表现为BBB运动功能评分和步态协调性显著提升，同时脊髓组织损伤范围明显缩小。在分子水平上，这2组脊髓组织中FOXP3、IL-10和TGF-β1的基因和蛋白表达显著上调，而RORγt、IL-17A和IL-6的表达则被显著抑制，这提示姜黄素干预肠道菌群后免疫平衡向Treg主导的抗炎状态倾斜。值得注意的是，联合使用GPRs抑制剂后，姜黄素修饰菌群带来的上述有益效应被逆转。 结论 本研究表明，姜黄素干预后的肠道菌群能够有效促进脊髓损伤后的运动功能恢复，其作用机制可能与激活GPRs信号通路，上调Treg细胞活性、抑制Th17细胞分化，最终纠正Treg/Th17免疫失衡密切相关。这为将姜黄素及其修饰后的肠道菌群作为脊髓损伤的辅助治疗策略提供了新的实验依据和应用价值。

姜黄素  /  肠道菌群  /  短链脂肪酸  /  脊髓损伤

Objective The immunoinflammatory response induced by spinal cord injury is a key factor hindering the recovery of neurological functions. Recent studies have shown that gut microbiota dysbiosis can participate in the immune regulation of the central nervous system through the gut-spinal cord axis. This study aims to explore whether curcumin can exert its protective effect on spinal cord injury by reshaping the gut microbiota and thereby regulating the local Treg/Th17 balance in the spinal cord. Methods Female Sprague-Dawley rats weighing 200‒220 g were randomly assigned into the sham operation group, spinal cord injury group, curcumin group, fecal microbiota transplantation group, fecal microbiota transplantation+ curcumin group, and fecal microbiota transplantation+curcumin+GPR inhibitor group. Neurological function recovery was evaluated based on the Basso-Beattie-Bresnahan motor function score and gait analysis. Histopathological changes in the injured area were observed via hematoxylin-eosin staining, Nissl staining, and Luxol Fast Blue staining. RT-qPCR, ELISA, and Western blotting were employed to quantify the expression levels of key transcription factor forkhead box protein 3 (FOXP3) for Treg cells, anti-inflammatory cytokines interleukin (IL)-10 and transforming growth factor (TGF)-β1, as well as key transcription factor retinoic acid receptor-related orphan receptor gamma t (RORγt) for Th17 cells and pro-inflammatory cytokines IL-17 and IL-6 in the spinal cord of each group. Results Compared with the spinal cord injury group and fecal microbiota transplantation group, the curcumin group and fecal microbiota transplantation+ curcumin group showed the most significant improvement in neurological function, specifically manifested by significant increases in BBB motor function scores and gait coordination, along with a marked reduction in the scope of spinal cord injury. At the molecular level, the two groups showed significantly upregulated gene and protein levels of FOXP3, IL-10, and TGF-β1 and significantly inhibited expression of RORγt, IL-17A, and IL-6 in the spinal cord tissue. This suggests that after curcumin intervention in the gut microbiota, the immune balance shifted toward a Treg-dominated anti-inflammatory state. Notably, the aforementioned beneficial effects of curcumin-modified gut microbiota were reversed after combined use of the GPR inhibitor. Conclusion This study indicates that curcumin can act on the gut microbiota to promote the recovery of motor function after spinal cord injury. Curcumin may exert the effect by activating the GPR signaling pathway, thereby upregulating Treg viability, inhibiting Th17 differentiation, and ultimately correcting the Treg/Th17 imbalance. This provides new experimental evidence and application value for using curcumin and its modified gut microbiota as an adjuvant therapeutic strategy for spinal cord injury.

curcumin  /  gut microbiota  /  short-chain fatty acids  /  spinal cord injury
田春平, 吴佳俊, 肖林峰, 王青燕, 杜嘉妮, 胡倩倩, 强京灵, 常小卫, 杨彦玲. 姜黄素通过肠道菌群调节Treg/Th17平衡改善脊髓损伤. 微生物学报, 2026 , 66 (5) : 2416 -2429 . DOI: 10.13343/j.cnki.wsxb.20250698
Chunping TIAN, Jiajun WU, Linfeng XIAO, Qingyan WANG, Jiani DU, Qianqian HU, Jingling QIANG, Xiaowei CHANG, Yanling YANG. Curcumin ameliorates spinal cord injury by regulating the Treg/Th17 balance via gut microbiota[J]. Acta Microbiologica Sinica, 2026 , 66 (5) : 2416 -2429 . DOI: 10.13343/j.cnki.wsxb.20250698
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脊髓损伤(spinal cord injury, SCI)是一种严重的创伤性中枢神经系统疾病，通常由外力对脊髓或脊髓周围结构造成损害而引发，其临床表现为感觉、运动和自主神经功能障碍，严重影响患者的生活质量和日常功能[1-2]。脊髓损伤可分为原发性脊髓损伤和继发性脊髓损伤，继发性脊髓损伤包括脂质过氧化、神经胶质细胞激活、神经炎症和氧化应激等，其中神经炎症被认为是导致脊髓继发性损伤加重的关键因素[3-5]。因此，抑制脊髓损伤后神经细胞炎症的发生是治疗成功的关键。
辅助性T细胞17 (T helper cell 17, Th17 cell)是CD4+ T细胞的一个亚群，白细胞介素-6 (interleukin-6, IL-6)通过信号转导与转录激活因子3 (signal transducer and activator of transcription, STAT3)诱导视黄醇相关孤儿受体γt (retinoid-related orphan receptor gamma t, RORγt)转录，促进Th17细胞的增殖和分化，产生更多的白细胞介素-17A (interleukin-17A, IL-17A)等促炎细胞因子，进而介导炎症反应和自身免疫性疾病的发生发展[6-7]。调节性T细胞(regulatory T cells, Treg cell)是CD4+ T细胞的另一个亚群，转化生长因子-β (transforming growth factor-β, TGF-β)诱导叉头样转录因子3 (forkhead box P3, FOXP3)转录，促进Treg细胞的增殖和分化，使其分泌白细胞介素-10 (interleukin-10, IL-10)等抗炎细胞因子，发挥免疫抑制作用[8-9]。在正常生理状态下Treg/Th17细胞处于动态平衡，共同维持机体的免疫稳态[10]。然而，在脊髓损伤等病理状态下这种平衡被打破，Th17细胞功能亢进，Treg细胞功能相对不足，导致过度炎症反应，加重脊髓损伤[11-12]。因此，调节Treg/Th17平衡成为治疗脊髓损伤的潜在靶点。
肠道菌群作为人体重要的“微生物器官”，近年来被发现与机体免疫系统及神经系统存在密切联系[13-14]。肠道菌群失衡不仅会影响肠道局部免疫，还可通过“肠-脑轴”影响中枢神经系统的免疫和炎症状态[15-16]。研究发现，肠道菌群可通过代谢产物及其衍生物与宿主相互作用，其中菌群代谢产生的芳香烃受体激动剂、短链脂肪酸(short chain fatty acids, SCFAs)及菌群衍生物脂多糖等对中枢神经系统炎症具有重要的调节作用[17-19]。SCFAs是肠道菌群重要的代谢产物之一，正常人肠道每天产生的SCFAs为50-100 mmol，由肠道产生的SCFAs不仅是宿主肠上皮细胞的首选能量代谢原料和细胞增殖分化的主要调控因子，还具有抗氧化、抗炎、抗肿瘤以及调控基因表达、调控宿主肠道免疫、改善肠道功能等多种重要作用[19-21]。已有文献报道，肠道菌群代谢产物SCFAs可与细胞表面的G蛋白偶联受体结合，通过调节Treg/Th17平衡调控宿主的免疫应答[22-24]。
姜黄素是一种从姜科植物根茎中分离出的黄橙色天然多酚类物质，具有抗炎、抗氧化、抗肿瘤和抑制细胞凋亡的作用[25-26]。研究发现，姜黄素在脊髓损伤[27]、阿尔茨海默病[28]、帕金森病[29]等中枢神经系统疾病中具有显著的神经保护功能。此外，课题组前期研究表明，姜黄素在促进脊髓损伤修复的过程中能显著重塑肠道微生物群的结构和丰度，并提升其代谢产物SCFAs的水平[30-31]。基于以上研究基础，提出科学假说(图1)，姜黄素可能通过调控肠道菌群提高SCFAs的水平，进而影响Treg/Th17平衡，最终发挥其对脊髓损伤的修复作用。为此，本研究通过粪菌移植实验，结合实时荧光定量逆转录PCR检测(real-time RT-qPCR, RT-qPCR)、酶联免疫吸附(enzyme-linked immunosorbent assay, ELISA)和蛋白印迹分析(Western blotting)等技术，检测脊髓局部Treg和Th17细胞相关转录因子及炎症因子的表达，探讨姜黄素干预后的肠道菌群改善脊髓损伤的具体机制，为临床应用姜黄素治疗脊髓损伤提供理论基础和实验依据。
1 材料与方法
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1.1 动物及实验分组
Specific pathogen free (SPF)级健康雌性SD大鼠，6周龄，体重200-220 g，购自西安交通大学，动物许可证：SCXK(陕)2018-001。大鼠置于动物房，室温25 ℃左右，适应性饲养2周，自由进食进水，每天给予大鼠12 h光照/12 h黑暗环境。先用随机数字表将动物分为2组：对照组和姜黄素(curcumin, CUR)组，每组8只。按照之前的经验，实验组每只大鼠每天灌胃100 mg/kg的姜黄素(Sigma-Aldrich公司)，对照组不做处理。于灌胃后的第14天收集新鲜粪便进行后续实验。然后，再用随机数字表将动物分为5组，分别为假手术(sham operation, Sham)组、脊髓损伤(SCI)组、姜黄素组、粪菌移植(fecal microbiota transplantation, FMT)组、粪菌移植姜黄素(FMT+CUR)组，粪菌移植姜黄素加抑制剂(FMT+CUR+GLPG0974)组，每组各5只，假手术组仅打开椎板以暴露硬脊膜，不进行脊髓损伤操作(图2)。FMT组和FMT+CUR组，参考Tian等[32]的方法，进行为期2周的抗生素处理以清除原有肠道菌群后，行脊髓损伤术，术后每2 d灌胃1 mL供体粪便上清液。FMT+CUR+GLPG0974组，参考Akiba等[33]的方法加入抑制剂并确定给药量。若试验过程中出现动物死亡情况，无法完成实验时应及时补充并重新制作模型。本研究所有动物实验获得延安大学动物伦理委员会批准，编号为S-S20240038。
1.2 脊髓损伤模型建立
正式造模前，将所用手术器械和医用耗材进行无菌处理，同时准备医用酒精、碘伏、生理盐水、2%戊巴比妥钠(上海山浦化工有限公司)、氨苄青霉素钠(武汉赛维尔生物科技有限公司)等。术前12 h大鼠禁食、禁水，正式造模在无菌环境下进行。将大鼠用戊巴比妥钠(15-40 mg/kg)进行腹腔麻醉，确定大鼠麻醉后，将其以俯卧位固定于操作台上，手指触摸寻找T10棘突，判断T10棘突位置，以此为中心，半径3-5 cm备皮。消毒后于此处切开皮肤约1.5 cm，使用镊子、止血钳和眼科剪将浅筋膜及棘突边缘两侧竖脊肌和韧带分离。根据棘突方向确定T10位置：T9棘突朝向尾侧，T10棘突呈中立位，T11棘突朝向头侧。使用止血钳提起T10棘突，并使用眼科剪逐步且轻缓地剪开T10和T11椎板之间的韧带。最后，利用精细咬骨钳逐步咬除T10椎板，从而暴露硬脊膜。将大鼠稳固于打击器台面，使用IH-0400脊髓打击器对T10进行力度为200千达因的打击。打击成功后，脊髓被打击部位出现充血现象，同时大鼠出现短暂的呼吸骤停，尾部出现摆尾反射，双下肢及躯体回缩样扑动，麻醉清醒后双下肢呈弛缓性瘫痪。将大鼠肌肉和皮肤逐层缝合，伤口消毒3次。对大鼠双后肢注射5 mL生理盐水，任意一侧后肢肌内注射青霉素钠4×105 U/支，将大鼠置于电热毯上，待其苏醒后回笼饲养，每天3次人工排尿，直至大鼠实现自主排尿。保持12 h光照/12 h黑暗，动物房温度控制在25 ℃左右。
1.3 抗生素溶液
分别准确称量硫酸新霉素1 g、盐酸万古霉素0.5 g、氨苄青霉素钠1 g和甲硝唑1 g，充分溶解于900 mL去离子水中，定容至1 L，4 ℃保存备用[34]。
1.4 粪菌移植
收集的新鲜粪便，浸泡在无菌PBS (1粪便颗粒/mL)中约15 min，匀浆，4 ℃、1 000 r/min离心5 min以沉淀颗粒物，收集悬浮液，4 ℃、8 000 r/min离心5 min以获得总细菌，将最终细菌悬浮液与终浓度为20%无菌甘油混合，然后储存在-80 ℃直至移植。调整悬浮液浓度，使其OD600值为0.5，在无菌PBS中对应约108 CFU/mL[35]。
1.5 运动功能测试
根据BBB运动评定量表[36]评分评估后肢运动功能的恢复。该量表基于让大鼠在100 cm的场地中自由行走5 min，同时密切观察后肢的运动和协调性。Sham组、SCI组、FMT组和FMT+CUR组分别于术后1、3、5、7、14、21和28 d进行评估。该评分由2位熟练掌握细则但不参与本研究的其他人员进行，评估重复3次并立即记录。分数范围从0到21，其中0表示无运动功能，21表示正常。术后28 d进行足迹分析以评估步态和运动协调性[37]。在老鼠的前肢和后肢上涂上不同颜色的染料，然后将老鼠放在白纸上让其进行直线行走，重复实验3次并记录。
1.6 组织制备
术后28 d，每组大鼠麻醉后灌注生理盐水。然后取损伤点上方和下方2 cm的脊髓，并在4%多聚甲醛(武汉赛维尔生物科技有限公司)中固定48 h。梯度脱水后，将样品包埋在石蜡中，并切成10 μm厚的切片。
1.7 苏木精-伊红染色、尼氏染色和劳克坚牢蓝染色
按照苏木精-伊红染色(hematoxylin-eosin staining, HE)、尼氏染色(Nissl)和劳克坚牢蓝染色(Luxol Fast Blue, LFB)试剂盒(Solarbio公司)的说明书，对切片进行染色，然后用梯度乙醇逐级脱水，最后将载玻片用二甲苯透明化，并用中性树胶(上海标本模型厂)封片。
1.8 实时荧光定量逆转录PCR检测
使用M5 Total RNA Extraction Reagent (TRIgent) (北京聚合美生物科技有限公司)按照说明书从大鼠脊髓中分离提取总RNA，用RNA逆转录酶反转录为cDNA，RT-qPCR检测β-actin、IL-17A、IL-6、RORγt、TGF-β1和FOXP3的Ct值。PCR反应体系(20 μL)：Hieff® qPCR SYBR Green Master Mix (High Rox Plus) 10 µL，上、下游引物(10 µmol/L)各0.4 µL，DNA模板2 µL，ddH2O 7.2 µL。PCR反应条件：95 °C预变性5 min；95 °C变性10 s，60 °C退火20 s，72 °C延伸20 s，40个循环。反应使用2-∆∆Ct方法计算基因的相对表达量[38]。PCR引物设计：从GenBank数据库检索大鼠源β-actin、IL-17A、IL-6、RORγt、TGF-β1和FOXP3 mRNA序列号及相应序列，设计PCR引物如表1所示。
1.9 酶联免疫吸附测定
称取脊髓组织，放入900 mL生理盐水中，超声研磨并以3 000 r/min离心10 min以获得脊髓组织匀浆。细胞因子包括IL-10、IL-6 (武汉三鹰生物技术有限公司)、IL-17A (深圳欣博盛生物科技有限公司)，根据说明书通过ELISA试剂盒进行测量。最后，使用酶标仪检测吸光度值。根据标准曲线获得各细胞因子的浓度。
1.10 蛋白印迹分析
使用RIPA裂解缓冲液(上海碧云天生物技术股份有限公司)从脊髓组织中提取总蛋白样品，通过BCA蛋白检测试剂盒(武汉博士德生物工程有限公司)定量提取物中的蛋白质浓度，确定上样量后将每组样品上到凝胶中电泳，电泳结束后进行PVDF (Merck Millipore公司)转膜，5%脱脂奶粉(内蒙古伊利实业集团股份有限公司)封闭2 h后孵育一抗FOXP3抗体、IL-17A抗体、TGF-β1抗体(江苏亲科生物研究中心有限公司)；RORγt抗体购自武汉博士德生物工程有限公司，4 ℃过夜孵育二抗(抗鼠、抗兔)，洗膜后，用化学发光试剂(北京索莱宝科技有限公司)观察蛋白质条带，最后通过ImageJ软件分析条带强度，并归一化为β-肌动蛋白(武汉三鹰生物技术有限公司)的强度。
1.11 数据分析和统计
使用GraphPad Prism 8.0软件进行数据的统计分析及绘图。所有的实验结果均重复3次及以上后获得，数据结果以平均数±标准差展示，2组数据之间的比较使用独立样本t检验，多组数据之间的比较使用单因素方差分析后，使用Tukey’s检验进行两两比较。P<0.05为差异有统计学意义。
2 结果与分析
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2.1 姜黄素干预后的肠道菌群对脊髓损伤大鼠运动功能和组织形态的影响
为探究姜黄素干预后的肠道菌群对脊髓损伤大鼠运动功能和组织形态的影响，本研究开展了粪菌移植实验。将灌有姜黄素处理和正常饲养大鼠粪便的悬浮液灌饲至脊髓损伤大鼠体内，依据BBB评分量表评估大鼠SCI后双后肢运动功能恢复情况。BBB评分结果显示，脊髓损伤后各组大鼠的评分均降为0分；随着时间的推移，SCI组、CUR组、FMT组和FMT+CUR组的评分逐渐增加，且CUR组和FMT+CUR组的评分明显高于其他2组，但各组评分依低于Sham组(图3A)。步态分析结果显示，脊髓损伤后大鼠前、后爪运动协调性显著下降；与SCI组相比，CUR组、FMT组和FMT+CUR组大鼠后爪的步幅更长、后肢拖拽更短，表明其步态恢复更快、运动协调性更好(图3B-3C)。HE染色结果显示，脊髓损伤后4周，CUR组和FMT+CUR组的损伤区域和空洞明显少于SCI组和FMT组；Nissl染色结果显示，CUR组和FMT+CUR组神经元数量多于SCI组和FMT组；LFB染色结果显示，CUR组和FMT+CUR组髓鞘密度大于SCI组和FMT组(图3D-3G)。以上数据表明，姜黄素干预后的肠道菌群能显著促进脊髓损伤大鼠的运动功能和组织形态学恢复。
2.2 姜黄素干预后的肠道菌群对Treg和Th17细胞的影响
为探究姜黄素干预后的肠道菌群对Treg和Th17细胞的影响，分别检测脊髓组织中Treg和Th17细胞相关转录因子FOXP3、RORγt及炎症因子IL-10、TGF-β1、IL-17A和IL-6[39]在RNA和蛋白水平的表达。结果发现，在RNA水平上，与SCI组和FMT组相比，FMT+CUR组的FOXP3、IL-10和TGF-β1的表达明显升高，而RORγt、IL-17A和IL-6的表达明显降低(图4A-4F)。在蛋白水平上，采用ELISA和Western blotting 2种方法进行检测。ELISA检测结果显示，与SCI组和FMT组相比，FMT+CUR组IL-10的表达明显升高，而IL-17A和IL-6的表达明显降低(图4G-4I)，Western blotting检测结果显示，与SCI组和FMT组相比，FMT+CUR组RORγt的表达明显降低，而FOXP3和TGF-β1的表达升高(图4J-4M、图5)，这些数据表明，经姜黄素干预后的肠道菌群可促进脊髓损伤大鼠体内Treg细胞的分化，同时抑制Th17细胞的活化。
2.3 姜黄素干预后的肠道菌群通过调节Treg/Th17平衡促进脊髓损伤恢复
据报道，短链脂肪酸可通过G蛋白偶联受体调节免疫细胞的分化[40]。实验结果表明，姜黄素可使短链脂肪酸中乙酸的浓度增加[30]，而乙酸又可与GPR43受体结合发挥免疫作用[41]。为进一步验证姜黄素是否通过肠道菌群调节短链脂肪酸中乙酸的浓度水平，进而影响Treg/Th17平衡，促进脊髓损伤修复，在粪菌移植的同时加入GPR43受体的抑制剂GLPG0974[33,42]。通过Western blotting和ELISA检测发现，加入抑制剂后Treg和Th17相关炎症因子及转录因子的表达发生逆转，RORγt、IL-17A和IL-6的蛋白表达升高，而FOXP3、TGF-β1和IL-10的表达降低(图5、图6A-6C)。基于以上数据，提出姜黄素通过短链脂肪酸调节Treg/Th17平衡促进脊髓损伤的恢复。
3 讨论与结论
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本研究通过体内实验系统探究了姜黄素、肠道菌群与Treg/Th17平衡之间的复杂调控关系在脊髓损伤修复中的关键作用。这一发现为神经-免疫-肠道菌群轴在脊髓损伤修复中的作用机制提供了新的实验依据。传统的神经损伤修复研究主要聚焦于神经细胞自身的再生能力、神经生长因子的作用以及炎症反应对神经组织的直接影响等方面，而本研究将研究视角拓展到了肠道菌群这一新兴领域。研究发现，姜黄素能够重塑肠道菌群结构，增加有益菌的丰度，减少有害菌的数量，进而改善肠道微生态环境。这种改变不仅局限于肠道局部，还通过一系列复杂的信号传导机制，远程调控机体的免疫反应，特别是对Treg/Th17平衡进行精准调节。这一过程涉及肠道菌群代谢产物的介导作用，如短链脂肪酸等物质在免疫细胞分化和功能调节中发挥关键作用，为神经损伤修复过程中免疫调节机制的研究提供了全新视角。未来研究可从多个层面深入探究姜黄素的作用机制。在分子机制层面，应进一步研究姜黄素与肠道菌群之间的直接相互作用，明确姜黄素影响肠道菌群代谢和基因表达的具体分子靶点。通过高通量测序技术和代谢组学分析，全面揭示姜黄素干预后肠道菌群的基因表达谱和代谢产物谱的变化，筛选出关键的分子标志物和代谢通路。深入研究姜黄素调节Treg/Th17平衡过程中涉及的细胞内信号传导通路，如Wnt/β-catenin信号通路、Notch信号通路等的作用，明确这些信号通路之间的相互调控关系，为进一步阐明姜黄素的作用机制提供理论依据[43-44]。在细胞间通讯层面，研究肠道上皮细胞、免疫细胞与肠道菌群之间的信号交流在姜黄素调节Treg/Th17平衡中的作用。探索肠道上皮细胞如何感知肠道菌群的变化并将信号传递给免疫细胞，以及免疫细胞如何通过分泌细胞因子和趋化因子调节肠道菌群的组成和功能。在基因调控层面，利用基因编辑技术，如CRISPR/Cas9系统，研究关键基因在姜黄素调节脊髓损伤修复中的功能[45]。通过敲除或过表达相关基因，观察姜黄素对脊髓损伤修复、肠道菌群调节和Treg/Th17平衡的影响，深入揭示基因调控在这一过程中的作用机制。
基金
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  • 国家自然科学基金(82560280)
  • 国家自然科学基金(82560366)
  • 陕西省科学技术厅一般项目(2024SF-YBXM-037)
  • 延安市科学技术局项目(2024SLZDCY-021)
  • 延安大学教育创新计划(YCX2024102)
文献
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参考文献 引证文献
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2026年第66卷第5期
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doi: 10.13343/j.cnki.wsxb.20250698
  • 接收时间：2025-09-12
  • 首发时间：2026-05-09
  • 出版时间：2026-05-04
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  • 收稿日期：2025-09-12
  • 录用日期：2025-12-28
基金
The National Natural Science Foundation of China(82560280)
国家自然科学基金(82560280)
The National Natural Science Foundation of China(82560366)
国家自然科学基金(82560366)
The General Project of Shaanxi Provincial Department of Science and Technology(2024SF-YBXM-037)
陕西省科学技术厅一般项目(2024SF-YBXM-037)
The Project of Yan’an Science and Technology Bureau(2024SLZDCY-021)
延安市科学技术局项目(2024SLZDCY-021)
The Graduate Education Innovation Program of Yan’an University(YCX2024102)
延安大学教育创新计划(YCX2024102)
作者信息
    1.延安大学延安医学院，陕西 延安
    2.延安大学附属医院神经外科，陕西 延安
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
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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