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Article(id=1240730060110491754, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202411196, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1731168000000, receivedDateStr=2024-11-10, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1773742697979, onlineDateStr=2026-03-17, pubDate=1745510400000, pubDateStr=2025-04-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773742697979, onlineIssueDateStr=2026-03-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773742697979, creator=13701087609, updateTime=1773742697979, updator=13701087609, issue=Issue{id=1240730050669113883, tenantId=1146029695717560320, journalId=1227665162245664772, year='2025', volume='52', issue='8', pageStart='1345', pageEnd='1536', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773742695728, creator=13701087609, updateTime=1773742807836, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1240730520988995837, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1240730520988995838, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1476, endPage=1483, ext={EN=ArticleExt(id=1240730060425064579, articleId=1240730060110491754, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=Transcriptomics of nicotinamide mononucleotide ameliorating silica-induced lung injury in mice, columnId=1228016572065837304, journalTitle=Modern Preventive Medicine, columnName=Experimental Technology and Applications, runingTitle=null, highlight=null, articleAbstract=
Objective

To study the effect and mechanism of nicotinamide mononucleotide (NMN) in alleviating silica-induced lung injury, and to provide a new option for the adjuvant treatment of silicosis.

Methods

The male C57BL/6 mice were randomly divided into control group, SiO2 group, and NMN intervention group according to body weight, with 10 mice in each group. Mice were given SiO2 (50 mg/ml, 80 μl) by tracheal instillation to construct a mouse model of silicosis, and NMN (1 000 mg/kg) was given by gavage for 7 days and 28 days. Histopathological staining was used to assess lung lesions, and transcriptomic sequencing was used to analyze gene expression and screen for key genes.

Results

NMN intervention alleviated SiO2-induced lung injury. Gene clustering results showed that NMN intervention improved SiO2-induced gene expression disorders to a certain extent, and the improvement effect of 28 days was better than 7 days of NMN intervention. After 7 and 28 days of SiO2 exposure, 1 163 genes were up-regulated in the SiO2 group compared with the control group, and were down-regulated in the NMN group compared with the SiO2 group, of which 445 were differential genes. Similarly, 1 657 genes were down-regulated in the SiO2 group compared with the control group, and were up-regulated in the NMN group compared with the SiO2 group, of which 571 were differential genes. The main GO term of the above differential genes was RNA polymerase and transcriptional regulation, and main KEGG pathways were IL-17 signaling pathway (P<0.001), cytokine-cytokine receptor interaction (P<0.001), Th17 cell differentiation (P<0.001), TNF signaling pathway (P<0.001). According to the number of pathways involved in the regulation of differential genes, the TOP8 hub genes were Mapk11, Mapk12, Il1b, H2-Ob, Csf2, Shc2, Mmp9, Ccl25.

Conclusion

NMN alleviates lung injury in silicosis mice by regulating immunity.

, correspAuthors=Li-qun 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, authorCompany=null, fund=null, authors=null, authorsList=Zi-yi MA, Qiong-hua DING, Wen DU, Ding-zi ZHOU, Qin ZHANG, Li-jun PENG, Yong-mei XIE, Yu-qin YAO, Li-qun WANG), CN=ArticleExt(id=1240730061641412840, articleId=1240730060110491754, tenantId=1146029695717560320, journalId=1227665162245664772, language=CN, title=烟酰胺单核苷酸改善二氧化硅诱导小鼠肺损伤的转录组学研究, columnId=1228016572288135432, journalTitle=现代预防医学, columnName=实验技术及其应用, runingTitle=null, highlight=null, articleAbstract=
目的

研究烟酰胺单核苷酸（Nicotinamide mononucleotide，NMN）缓解二氧化硅（SiO2）诱导肺损伤的作用与机制，为矽肺的辅助治疗提供新的选择。

方法

雄性C57BL/6小鼠按体重随机分为对照组（Control组）、SiO2染尘组（SiO2组）、和NMN干预组（SiO2+NMN组），每组10只。通过单次非暴露式气管滴注法向小鼠滴注SiO2悬液（50 mg/ml, 80 μl）构建SiO2染尘模型；NMN干预组小鼠采用相同方法染尘后通过灌胃每日给予NMN（1 000 mg/kg），分别持续7天、28天。通过组织病理学染色观察肺部病变情况；采用转录组学测序分析肺组织基因表达谱，筛选关键基因。

结果

NMN干预减轻SiO2染尘小鼠的肺组织病变。基因聚类结果显示NMN干预能够在一定程度上改善染尘诱导的基因表达谱紊乱，在28天时改善效果更好。染尘7天和28天后，与对照组相比SiO2组上调、且与SiO2组相比NMN干预组下调的基因共有1 163个，其中445个为差异基因；染尘7天后和染尘28天后，与对照组相比SiO2组下调、且与SiO2组相比NMN干预组上调的基因共有1 657个，其中571个为差异基因。以上差异基因主要富集的GO条目为RNA聚合酶及转录调控等；KEGG通路为IL-17信号通路（P<0.001）、细胞因子-细胞因子受体相互作用（P<0.001）、Th17细胞分化（P<0.001）、TNF信号通路（P<0.001）等。按差异基因参与调控的通路数筛选出其中TOP 8的核心基因，为Mapk11、Mapk12、Il1b、H2-Ob、Csf2、Shc2、Mmp9、Ccl25。

结论

NMN通过调节免疫缓解SiO2染尘小鼠的肺损伤。

, correspAuthors=王礼群, authorNote=null, correspAuthorsNote=
王礼群，E-mail：
, copyrightStatement=本刊刊出的所有文章不代表中华预防医学会和本刊编委会的观点，除非特别声明。, copyrightOwner=中华预防医学会和四川大学华西公共卫生学院, extLink=null, articleAbsUrl=null, sourceXml=j7L4LYcifDqll9tbgT54jQ==, magXml=yxdOMeAvWMPAKqicqkOQ/A==, pdfUrl=null, pdf=2OlxxpS/uMTLgI/HmqUrcA==, pdfFileSize=3051387, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=VlMILGC4jhhX2Mq9KK54fQ==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=1DpK6szhsbQynW9hLcWciw==, mapNumber=null, authorCompany=null, fund=null, authors=

马子怡（2000—），女，硕士在读，研究方向：卫生毒理学

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马子怡（2000—），女，硕士在读，研究方向：卫生毒理学

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Macrophage differential genes and their functions in silicosis based on single cell RNA sequencing and spatial transcriptome sequencing[J]. Journal of Environmental and Occupational Medicine, 2022, 39(12): 1350-1358. (In Chinese), articleTitle=Macrophage differential genes and their functions in silicosis based on single cell RNA sequencing and spatial transcriptome sequencing, refAbstract=null), Reference(id=1241070743925092375, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, doi=null, pmid=null, pmcid=null, year=2020, volume=21, issue=21, pageStart=8412, pageEnd=null, url=null, language=null, rfNumber=[28], rfOrder=30, authorNames=Korbecki J, Kojder K, Simińska D, journalName=International Journal of Molecular Sciences, refType=null, unstructuredReference=Korbecki J, Kojder K, Simińska D, et al. CC chemokines in a tumor: a review of Pro-Cancer and Anti-Cancer properties of the ligands of receptors CCR1, CCR2, CCR3, and CCR4[J]. International Journal of Molecular Sciences, 2020, 21(21): 8412., articleTitle=CC chemokines in a tumor: a review of Pro-Cancer and Anti-Cancer properties of the ligands of receptors CCR1, CCR2, CCR3, and CCR4, refAbstract=null)], funds=[Fund(id=1241070740515124077, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, awardId=U22A20359, language=CN, fundingSource=国家自然科学基金(U22A20359), fundOrder=null, country=null), Fund(id=1241070740661924723, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, awardId=U23A20495, language=CN, fundingSource=国家自然科学基金(U23A20495), fundOrder=null, country=null), Fund(id=1241070740812919672, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, awardId=2023NSFSC1729, language=CN, fundingSource=四川省科技厅自然科学基金(2023NSFSC1729), fundOrder=null, country=null), Fund(id=1241070740917777278, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, awardId=2023NSFSC0649, language=CN, fundingSource=四川省科技厅自然科学基金(2023NSFSC0649), fundOrder=null, country=null)], companyList=[AuthorCompany(id=1241070732625637722, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=1., ext=[AuthorCompanyExt(id=1241070732638220636, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070732625637722, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan 610041, China), AuthorCompanyExt(id=1241070732654997855, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070732625637722, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=1.四川大学华西公共卫生学院/华西第四医院，卫生毒理与病理学系，四川　成都　610041)]), AuthorCompany(id=1241070732814381418, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=2., ext=[AuthorCompanyExt(id=1241070732818575722, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070732814381418, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=2.四川大学华西公共卫生学院/华西第四医院，尘肺科/呼吸与危重症医学科)]), AuthorCompany(id=1241070732944404854, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=3., ext=[AuthorCompanyExt(id=1241070732956987769, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070732944404854, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=3.四川大学华西公共卫生学院/华西第四医院，劳动卫生与环境卫生学系)]), AuthorCompany(id=1241070733074428291, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=4., ext=[AuthorCompanyExt(id=1241070733082816901, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070733074428291, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=4.四川大学华西医院，生物治疗国家重点实验室)]), AuthorCompany(id=1241070733233811856, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=5., ext=[AuthorCompanyExt(id=1241070733246394770, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070733233811856, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=5.成都川宇健维生物科技有限公司)]), AuthorCompany(id=1241070733363835292, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, xref=6., ext=[AuthorCompanyExt(id=1241070733376418207, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, companyId=1241070733363835292, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=6.四川大学华西公共卫生学院/华西第四医院，重大疾病医防融合研究所)])], figs=[ArticleFig(id=1241070739000980240, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Fig.1, caption=Histopathological stainingof 7day mice and 28day micewith NMN intervention, figureFileSmall=szzmyEuJW/wk/z9VQigXPg==, figureFileBig=XHcWv6reWx7gYQGNInLUfQ==, tableContent=null), ArticleFig(id=1241070739089060629, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=图1, caption=NMN干预7天和28天小鼠H&E染色结果

注：A为NMN干预7天小鼠肺组织H&E染色；B为NMN干预28天小鼠肺组织H&E染色。放大倍数为5×、20×。

, figureFileSmall=szzmyEuJW/wk/z9VQigXPg==, figureFileBig=XHcWv6reWx7gYQGNInLUfQ==, tableContent=null), ArticleFig(id=1241070739219084062, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Fig.2, caption=Heatmaps and Venn diagrams forgenes of 7dayand 28day mice with NMN intervention, figureFileSmall=6Ybu00V+GHBEd4/gXnaptg==, figureFileBig=EWizORNDU2v1k4kmMVXaFg==, tableContent=null), ArticleFig(id=1241070739302970145, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=图2, caption=NMN干预7天和28天小鼠基因的热图与韦恩图

注：A为NMN干预7天小鼠基因的聚类分析热图；B为NMN干预28天小鼠基因的聚类分析热图；C为NMN干预7天和28天小鼠肺组织中保护基因韦恩图；D为NMN干预7天和28天小鼠肺组织中抑制基因韦恩图。

, figureFileSmall=6Ybu00V+GHBEd4/gXnaptg==, figureFileBig=EWizORNDU2v1k4kmMVXaFg==, tableContent=null), ArticleFig(id=1241070739403633446, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Fig.3, caption=Enrichment analysis of common genes and PPI analysis of key differential genes, figureFileSmall=8GC/sbnHPREXQbUHf6NIZw==, figureFileBig=x0BpprHRbGhyhJJ32mj9PA==, tableContent=null), ArticleFig(id=1241070739491713839, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=图3, caption=共同基因的富集分析图和关键差异基因的PPI分析图

注：A为保护基因的GO富集分析；B为抑制基因的GO富集分析；C为保护基因的KEGG气泡图；D为抑制基因的KEGG气泡图；E为30个差异基因的PPI网络图；F为TOP8差异基因的PPI网络图。

, figureFileSmall=8GC/sbnHPREXQbUHf6NIZw==, figureFileBig=x0BpprHRbGhyhJJ32mj9PA==, tableContent=null), ArticleFig(id=1241070739621737270, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Table 1, caption=

Level 1 of KEGG terms for common genes

, figureFileSmall=null, figureFileBig=null, tableContent=
KEGG富集条目一级水平KEGG条目数量
人类疾病55
生物体系统48
环境信息处理19
代谢17
分子过程15
遗传信息处理11
总计165
), ArticleFig(id=1241070739714011965, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=表1, caption=

共同基因KEGG富集条目一级水平

, figureFileSmall=null, figureFileBig=null, tableContent=
KEGG富集条目一级水平KEGG条目数量
人类疾病55
生物体系统48
环境信息处理19
代谢17
分子过程15
遗传信息处理11
总计165
), ArticleFig(id=1241070739839841091, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Table 2, caption=

Level 2 of KEGG terms for common genes

, figureFileSmall=null, figureFileBig=null, tableContent=
KEGG富集条目二级水平KEGG条目数量
免疫系统16
内分泌系统12
神经系统6
消化系统5
感官系统2
生长发育2
环境适应2
排泄系统1
老化1
循环系统1
总计48
), ArticleFig(id=1241070739936310089, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=表2, caption=

共同基因KEGG富集条目二级水平

, figureFileSmall=null, figureFileBig=null, tableContent=
KEGG富集条目二级水平KEGG条目数量
免疫系统16
内分泌系统12
神经系统6
消化系统5
感官系统2
生长发育2
环境适应2
排泄系统1
老化1
循环系统1
总计48
), ArticleFig(id=1241070740024390476, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Table 3, caption=

Number of repetitions of differential genes in immune pathways

, figureFileSmall=null, figureFileBig=null, tableContent=
基因名称重复次数
Mapk119
Mapk128
Il1b6
H2-Ob5
Csf24
Mmp92
Shc22
Ccl252
S100a8、Il17rb、S100a9、Foxp3、Cxcr2、Gm10591、Adcy3、Grk3、Foxo3、Shc2、Cxcr1、Gprc6a、Rbpjl、Cd22、Cd79b、Cd19、Cd209a、Rapgef3、Tnfrsf13c、C6、Hc、Hspa1l1
), ArticleFig(id=1241070740125053778, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=表3, caption=

免疫相关通路中差异基因的重复次数

, figureFileSmall=null, figureFileBig=null, tableContent=
基因名称重复次数
Mapk119
Mapk128
Il1b6
H2-Ob5
Csf24
Mmp92
Shc22
Ccl252
S100a8、Il17rb、S100a9、Foxp3、Cxcr2、Gm10591、Adcy3、Grk3、Foxo3、Shc2、Cxcr1、Gprc6a、Rbpjl、Cd22、Cd79b、Cd19、Cd209a、Rapgef3、Tnfrsf13c、C6、Hc、Hspa1l1
), ArticleFig(id=1241070740200551255, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=EN, label=Table 4, caption=

Pathways containing key differential genes

, figureFileSmall=null, figureFileBig=null, tableContent=
通路名称包含的关键基因
IL-17信号通路Mapk12、Mapk11、Csf2、Mmp9、S100a8、S100a9、Il17rb、Il1b
细胞因子-细胞因子受体相互作用Il1b、Csf2、Ccl25、Tnfrsf13c、Cxcr1、Il17rb、Cxcr2
Th17细胞分化Mapk11、Mapk12、Il1b、H2-Ob、Foxp3
TNF信号通路Mapk11、Mapk12、Il1b、Csf2、Mmp9
), ArticleFig(id=1241070740284437341, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730060110491754, language=CN, label=表4, caption=

包含关键差异基因的通路

, figureFileSmall=null, figureFileBig=null, tableContent=
通路名称包含的关键基因
IL-17信号通路Mapk12、Mapk11、Csf2、Mmp9、S100a8、S100a9、Il17rb、Il1b
细胞因子-细胞因子受体相互作用Il1b、Csf2、Ccl25、Tnfrsf13c、Cxcr1、Il17rb、Cxcr2
Th17细胞分化Mapk11、Mapk12、Il1b、H2-Ob、Foxp3
TNF信号通路Mapk11、Mapk12、Il1b、Csf2、Mmp9
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烟酰胺单核苷酸改善二氧化硅诱导小鼠肺损伤的转录组学研究
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马子怡 1 , 丁琼桦 1 , 杜文 2 , 周丁子 2 , 张勤 3 , 彭莉君 2 , 谢永美 4, 5 , 姚于勤 1, 2, 3, 6 , 王礼群 6, *
现代预防医学 | 实验技术及其应用 2025,52(8): 1476-1483
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现代预防医学 | 实验技术及其应用 2025, 52(8): 1476-1483
烟酰胺单核苷酸改善二氧化硅诱导小鼠肺损伤的转录组学研究
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马子怡1, 丁琼桦1, 杜文2, 周丁子2, 张勤3, 彭莉君2, 谢永美4, 5, 姚于勤1, 2, 3, 6, 王礼群6, *
作者信息
  • 1.四川大学华西公共卫生学院/华西第四医院，卫生毒理与病理学系，四川　成都　610041
  • 2.四川大学华西公共卫生学院/华西第四医院，尘肺科/呼吸与危重症医学科
  • 3.四川大学华西公共卫生学院/华西第四医院，劳动卫生与环境卫生学系
  • 4.四川大学华西医院，生物治疗国家重点实验室
  • 5.成都川宇健维生物科技有限公司
  • 6.四川大学华西公共卫生学院/华西第四医院，重大疾病医防融合研究所

    • 马子怡（2000—），女，硕士在读，研究方向：卫生毒理学

通讯作者:

王礼群，E-mail：
Transcriptomics of nicotinamide mononucleotide ameliorating silica-induced lung injury in mice
Zi-yi MA1, Qiong-hua DING1, Wen DU2, Ding-zi ZHOU2, Qin ZHANG3, Li-jun PENG2, Yong-mei XIE4, 5, Yu-qin YAO1, 2, 3, 6, Li-qun WANG6, *
Affiliations
  • West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan 610041, China
出版时间: 2025-04-25 doi: 10.20043/j.cnki.MPM.202411196
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摘要
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目的

研究烟酰胺单核苷酸（Nicotinamide mononucleotide，NMN）缓解二氧化硅（SiO2）诱导肺损伤的作用与机制，为矽肺的辅助治疗提供新的选择。

方法

雄性C57BL/6小鼠按体重随机分为对照组（Control组）、SiO2染尘组（SiO2组）、和NMN干预组（SiO2+NMN组），每组10只。通过单次非暴露式气管滴注法向小鼠滴注SiO2悬液（50 mg/ml, 80 μl）构建SiO2染尘模型；NMN干预组小鼠采用相同方法染尘后通过灌胃每日给予NMN（1 000 mg/kg），分别持续7天、28天。通过组织病理学染色观察肺部病变情况；采用转录组学测序分析肺组织基因表达谱，筛选关键基因。

结果

NMN干预减轻SiO2染尘小鼠的肺组织病变。基因聚类结果显示NMN干预能够在一定程度上改善染尘诱导的基因表达谱紊乱，在28天时改善效果更好。染尘7天和28天后，与对照组相比SiO2组上调、且与SiO2组相比NMN干预组下调的基因共有1 163个，其中445个为差异基因；染尘7天后和染尘28天后，与对照组相比SiO2组下调、且与SiO2组相比NMN干预组上调的基因共有1 657个，其中571个为差异基因。以上差异基因主要富集的GO条目为RNA聚合酶及转录调控等；KEGG通路为IL-17信号通路（P<0.001）、细胞因子-细胞因子受体相互作用（P<0.001）、Th17细胞分化（P<0.001）、TNF信号通路（P<0.001）等。按差异基因参与调控的通路数筛选出其中TOP 8的核心基因，为Mapk11、Mapk12、Il1b、H2-Ob、Csf2、Shc2、Mmp9、Ccl25。

结论

NMN通过调节免疫缓解SiO2染尘小鼠的肺损伤。

矽肺  /  烟酰胺单核苷酸  /  转录组测序  /  免疫调控
Objective

To study the effect and mechanism of nicotinamide mononucleotide (NMN) in alleviating silica-induced lung injury, and to provide a new option for the adjuvant treatment of silicosis.

Methods

The male C57BL/6 mice were randomly divided into control group, SiO2 group, and NMN intervention group according to body weight, with 10 mice in each group. Mice were given SiO2 (50 mg/ml, 80 μl) by tracheal instillation to construct a mouse model of silicosis, and NMN (1 000 mg/kg) was given by gavage for 7 days and 28 days. Histopathological staining was used to assess lung lesions, and transcriptomic sequencing was used to analyze gene expression and screen for key genes.

Results

NMN intervention alleviated SiO2-induced lung injury. Gene clustering results showed that NMN intervention improved SiO2-induced gene expression disorders to a certain extent, and the improvement effect of 28 days was better than 7 days of NMN intervention. After 7 and 28 days of SiO2 exposure, 1 163 genes were up-regulated in the SiO2 group compared with the control group, and were down-regulated in the NMN group compared with the SiO2 group, of which 445 were differential genes. Similarly, 1 657 genes were down-regulated in the SiO2 group compared with the control group, and were up-regulated in the NMN group compared with the SiO2 group, of which 571 were differential genes. The main GO term of the above differential genes was RNA polymerase and transcriptional regulation, and main KEGG pathways were IL-17 signaling pathway (P<0.001), cytokine-cytokine receptor interaction (P<0.001), Th17 cell differentiation (P<0.001), TNF signaling pathway (P<0.001). According to the number of pathways involved in the regulation of differential genes, the TOP8 hub genes were Mapk11, Mapk12, Il1b, H2-Ob, Csf2, Shc2, Mmp9, Ccl25.

Conclusion

NMN alleviates lung injury in silicosis mice by regulating immunity.

Silicosis  /  Nicotinamide mononucleotide  /  RNA-seq  /  Immune regulation
马子怡, 丁琼桦, 杜文, 周丁子, 张勤, 彭莉君, 谢永美, 姚于勤, 王礼群. 烟酰胺单核苷酸改善二氧化硅诱导小鼠肺损伤的转录组学研究. 现代预防医学, 2025 , 52 (8) : 1476 -1483 . DOI: 10.20043/j.cnki.MPM.202411196
Zi-yi MA, Qiong-hua DING, Wen DU, Ding-zi ZHOU, Qin ZHANG, Li-jun PENG, Yong-mei XIE, Yu-qin YAO, Li-qun WANG. Transcriptomics of nicotinamide mononucleotide ameliorating silica-induced lung injury in mice[J]. Modern Preventive Medicine, 2025 , 52 (8) : 1476 -1483 . DOI: 10.20043/j.cnki.MPM.202411196
正文
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尘肺是在职业活动中长期吸入生产性粉尘并在肺内潴留而引起的以肺组织弥漫性纤维化为主要特征的疾病，其中，矽肺是尘肺的一种主要类型[1]。矽肺（Silicosis）也叫硅肺，是因长期吸入大量二氧化硅（SiO2）粉尘而引起的一种肺部疾病，主要病变特征是肺组织炎性细胞浸润、纤维化和硅结节形成。来自于Global Health Data Exchange（GHDx）的数据显示，2019年全球有超过12 900例死亡病例归因于矽肺[1]。1990至2019年，中国新发尘肺病类型仍以矽肺为主，占矽肺病发病的81%以上[2]，给我国公共卫生体系带来沉重的负担。
矽肺发病机制复杂，现有研究假说认为，先天免疫和适应性免疫系统的激活在矽肺的早期阶段起着关键作用。经呼吸道进入肺组织中的SiO2会对细胞造成损伤，激活免疫系统从而介导巨噬细胞吞噬SiO2粉尘，并释放细胞因子促进损伤修复[3-4]。但由于粉尘无法被完全清除，粉尘诱导的系列炎性级联反应持续存在，导致组织修复过度，最终形成肺纤维化[5]。由此可见，矽肺的发生和进展伴随着免疫失衡和持续的炎性损伤。然而，矽肺的发生涉及多种细胞与细胞、细胞与微环境以及分子与分子之间的相互作用，针对单一或有限分子的研究难以准确阐述矽肺发生发展的分子机制。转录组学技术是对生物样本中所有基因表达与变化情况进行分析的一种高通量技术，在矽肺致病机制与药物研究中已取得一定进展[6-8]，对于矽肺发病机制研究与治疗靶点筛选具有重要作用。
矽肺致病机制不清阻碍了特效治疗药物的研发，目前的临床治疗方案主要是对症治疗。小分子靶向药物如尼达尼布和汉防己甲素已应用于矽肺的临床治疗，但疗效仍不理想[9-11]；在临床前研究中，抗细胞因子、抗氧化剂、影响自噬溶酶体系统的药物、增加环腺苷水平的药物以及一些特异性microRNA等均可抑制SiO2诱导的肺损伤[12]。然而，上述药物大多针对矽肺的具体症状，疗效有限且可能伴随一定的副作用，安全有效的矽肺治疗药物仍然缺乏。烟酰胺单核苷酸（Nicotinamide Mononucleotide, NMN）是一种烟酰胺腺嘌呤二核苷酸（Nicotinamide Adenine Dinucleotide, NAD+）的直接前体和高效补充剂。研究表明，在细胞内NAD+及其代谢产物是白细胞Ca2+信号转导所必需的第二信使[13]，这些信号分子在调节先天免疫和适应性免疫中发挥着重要作用，表明NAD+及其代谢物可以对多种免疫调节途径产生影响。既往研究表明，连续7天和28天给予C57BL/6小鼠500 mg/kg和1 000 mg/kg的NMN干预能显著减轻SiO2诱导的肺部病变，组织病理学上表现为肺重系数降低，肺组织中炎性细胞募集和浸润减少，并且NMN可以通过降低活性氧水平和增加谷胱甘肽水平来减轻SiO2诱导的氧化损伤[14]，但NMN在矽肺中的作用与机制尚不清楚。
综上，本研究将使用SiO2构建染尘小鼠模型，利用转录组测序分析染尘小鼠肺组织基因表达谱的变化，并筛选NMN缓解矽肺损伤的关键基因，全面解析NMN减轻肺损伤的机制，为将NMN用于矽肺的临床辅助治疗提供初步线索。
1　材料与方法
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1.1　动物与实验样本
6~8周龄的雄性C57BL/6小鼠购自北京维通利华实验动物技术有限公司，饲养于四川大学华西公共卫生学院/华西第四医院实验动物中心。本研究方案已通过四川大学华西公共卫生学院/华西第四医院动物伦理委员会的批准（No：Gwll2021073）。
1.2　主要试剂耗材
NMN购自成都川宇健维生物科技有限公司；SiO2购自美国西格玛-奥德里奇公司；Trizol试剂购自美国赛默飞生物科技公司；4%多聚甲醛购自合肥白鲨生物科技有限公司；生物分析仪2100和RNA 6000 Nano试剂盒购自美国安捷伦公司；动物总RNA分离试剂盒购自成都福际生物技术有限公司；Taq Pro Universal SYBR q-PCR预混液购自南京诺唯赞生物科技股份有限公司；含gDNA去除剂的qPCR用ABScript III RT预混液购自武汉爱博泰克生物科技有限公司。
1.3　方法
1.3.1　动物分组、造模及给药方法
将小鼠按体重随机分为对照组（Control组）、SiO2染尘组（SiO2组）、和NMN干预组（SiO2+NMN组），每组10只动物。通过单次非暴露式气管滴注法向小鼠滴注SiO2悬液（50 mg/ml, 80 μl）[15]构建SiO2染尘模型；NMN干预组小鼠采用相同方法染尘后通过灌胃每日给予NMN（1 000 mg/kg）[14,16-17]，分别持续7天、28天，每三天记录一次小鼠体重。
1.3.2　样本收集
分别于第7天、第28天行颈椎脱臼法处死小鼠，解剖取肺组织，部分肺组织固定于组织固定液中，用于组织学染色；剩余肺组织用液氮快速冷冻后放在-80℃冰箱中保存备用。
1.3.3　小鼠肺组织病理学染色
采用苏木精伊红染色法（Hematoxylin- Eosin staining，H&E）观察肺组织病理变化，用4%多聚甲醛固定组织，24小时后制作石蜡切片，在染色前用梯度醇溶液对切片进行脱蜡后依次用苏木精溶液和伊红染色液染色，梯度醇溶液脱水后置于二甲苯中透明，最后用中性树脂密封切片。使用病理大组织全切片扫描系统观察肺组织的病变情况。
1.3.4　小鼠肺组织转录组学测序
使用Trizol试剂对总样品的RNA进行分离和纯化，通过质控、完整性检测、琼脂糖电泳后对带有多聚腺苷酸的mRNA进行特异性捕获，利用镁离子对其片段化后通过逆转录酶合成cDNA同时掺入dUTP Solution，经UDP酶消化后通过PCR形成片段大小为（300±5） bp的文库，使用illuminaNovaseqTM 6000进行双端测序。
1.3.5　小鼠肺组织转录组学分析
使用omicstudio分析平台（https://www.omicstudio.cn/tool.）对数据进行分析，以FPKM值表示基因表达水平（界值P<0.05），以-log10（P-value）值绘制热图；筛选与对照组相比SiO2组上调、且与SiO2组相比NMN组下调的差异基因为发挥促进保护作用的基因，定义为保护基因，与对照组相比SiO2组下调、且与SiO2组相比NMN组上调的差异基因为发挥抑制保护作用的基因，定义为抑制基因，绘制韦恩图；对二者的共同基因进行GO和KEGG富集分析筛选出富集通路；对共同KEGG通路中的基因进行蛋白质相互作用（Protein-Protein Interaction，PPI）网络分析筛选出关键基因。
1.3.6　统计分析
计数资料用()表示，采用GraphPadPrism 8软件进行统计处理。差异基因的富集分析采用超几何检验，检验水准α=0.05。
2　结果
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2.1　NMN改善染尘小鼠的肺组织损伤
小鼠肺组织H&E染色结果如图1A、1B所示，与对照组相比，染尘7天后肺泡壁增厚，肺泡完整性破坏，可见炎性细胞浸润，NMN干预后小鼠肺组织病变程度减轻；染尘28天后，肺组织中可见炎性细胞结节形成，伴纤维细胞增生，与SiO2暴露7天相比，暴露28天后小鼠肺组织的正常区域进一步减少，NMN干预抑制SiO2诱导的肺组织病变，提示NMN干预缓解SiO2诱导的肺损伤。
2.2　NMN干预改善染尘小鼠肺组织基因表达谱的紊乱
如图2A、2B所示，基因聚类热图显示染尘导致肺组织整体基因表达谱发生明显变化，而NMN干预能够在一定程度上改善染尘诱导的基因表达谱紊乱，并且在28天时，改善效果更好。图2C、2D显示染尘7天后，与对照组相比SiO2组上调、且与SiO2组相比NMN组下调的保护基因共2 970个，染尘28天后共11 878个，二者取交集后有1 163个共同基因，其中445个为差异基因，718个为非差异基因；染尘7天后与对照组相比SiO2组下调、且与SiO2组相比NMN组上调的抑制基因共7770个，染尘28天后共5 440个，二者取交集后共有1 657个共同基因，其中571个为差异基因，1 086个为非差异基因。
2.3　NMN通过免疫调节缓解染尘小鼠的肺损伤
对上述共同基因进行富集分析，GO分析结果如图3A、3B所示，保护基因的差异基因富集在生物过程的条目为DNA为模板的转录调控、RNA聚合酶II对转录的正向调节、多细胞生物的发育、信号转导等；富集在细胞组分的条目为细胞膜、细胞质、膜的组成部分、细胞核等；富集在分子功能的条目为蛋白质结合、金属离子结合、相同蛋白质结合、DNA结合等。在抑制基因的差异基因中，富集在生物过程的条目为细胞周期、以DNA为模板的转录调控、信号转导、RNA聚合酶II对转录的正向调节等；富集在细胞组分的条目为细胞质、细胞核、细胞膜、细胞质等；富集在分子功能的条目为蛋白质结合、金属离子结合、核苷酸结合、ATP结合等。上述结果表明NMN通过调控DNA结合、RNA聚合酶及转录等过程缓解SiO2染尘小鼠肺损伤。
KEGG分析结果如图3C、3D所示，保护基因的差异基因主要富集在丝裂原活化蛋白激酶（Mitogen-activated Protein Kinase, MAPK）信号通路（P<0.001）、IL-17信号通路（P<0.001）、肿瘤坏死因子（Tumor Necrosis Factor, TNF）信号通路（P<0.001）、辅助性T细胞17（T Helper Cell 17, Th17）细胞分化（P<0.001）等；抑制基因的差异基因主要富集在细胞因子-细胞因子受体相互作用（P<0.001）、自然杀伤细胞介导的细胞毒性（P<0.001）、抗原呈递和表达（P<0.001）、原发性免疫缺陷（P<0.001）等。如表1、2所示，二者取交集后共筛选出165条共同KEGG通路，其中生物系统相关的KEGG通路数目仅次于人类疾病，这些通路中与免疫系统相关的通路数目又为最多。表3中，这些免疫系统相关KEGG通路中共包含30个重复差异基因，按差异基因参与调控的通路数筛选出其中TOP8基因，包括Mapk11、Mapk12、Il1b、H2-Ob、Csf2、Shc2、Mmp9、Ccl25。表四中反向分析后发现30个重复差异基因主要在IL-17信号通路、细胞因子-细胞因子受体相互作用、Th17细胞分化、TNF信号通路等通路中表达。PPI分析结果如图3E、3F所示，基于现有的研究报道和数据库分析表明，TOP8基因中有6个相互作用较为密切。以上结果提示NMN可以通过免疫调节缓解SiO2染尘小鼠肺损伤。
3　讨论
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本研究结果表明，NMN干预能有效减轻SiO2诱导的肺损伤，表现为肺组织病变减轻，基因表达谱部分恢复。组织病理学染色是评价肺组织病变程度的金标准，既往研究表明，NMN干预能够减轻颗粒物诱导的小鼠肺组织炎性细胞浸润和胶原沉积，从而缓解肺纤维化[18]。在博来霉素诱导的肺纤维化小鼠中，NMN干预也能减轻肺泡结构破坏的程度和肺间质炎性浸润程度[19]，与本研究观察到的结果相似。免疫调控是矽肺发生和进展的驱动因素，贯穿矽肺发展的整个病程，本研究的转录组学结果表明，NMN主要通过调节免疫缓解SiO2诱导的肺损伤。已有研究报道了NMN在免疫调节中的作用，NMN可通过激活IDO-kynurenine-AhR通路来抑制巨噬细胞的炎性损伤，而巨噬细胞与免疫调节密切相关[20]。此外，NMN还可以抑制CD4+T细胞的激活，并增强嵌合抗原受体T细胞免疫疗法（Chimeric Antigen Receptor T-Cell Immunotherapy, CAR-T）治疗的效果，是一种潜在的抗病毒辅助制剂[21]。上述研究进一步证实了NMN的免疫调节作用，此前已有临床研究证实NMN具有良好的安全性[22]，因此，NMN可能是一种潜在的免疫调节辅助剂，可作为矽肺临床辅助治疗剂的一种选择。
除矽肺外，SiO2暴露还与许多自身免疫性疾病有关，流行病学研究发现SiO2吸入与系统性红斑狼疮、类风湿性关节炎、原发性系统性血管炎、韦格纳肉芽肿病和系统性硬化症的发生密切相关[23]，与另一项关于SiO2相关肺病患者的风湿病并发症的评价结果一致[24]，提示免疫调控在矽肺发展中的重要作用。本研究从转录组学角度出发，筛选了7天和28天小鼠染尘后的1 163个共同保护基因，以及1 657个共同抑制基因，共2 820个共同基因，表明NMN干预可以在一定程度上纠正肺组织基因表达的紊乱。信号机制上，富集分析后发现这些共同基因主要富集的GO条目为RNA聚合酶及转录调控等，KEGG通路为IL-17信号通路、细胞因子-细胞因子受体相互作用、Th17细胞分化、TNF信号通路等，研究表明细胞因子与细胞因子受体结合后可传递信号，并参与免疫反应的调控，如IL-17细胞因子及TNF在免疫调节、免疫抑制和免疫效应的功能中起着重要作用[6,25]，而Th17细胞可以通过分泌IL-17从而介导免疫反应[26]。对上述共同基因进行分析后筛选出30个共同差异基因，按差异基因参与调控的通路数筛选出TOP 8基因，包括Ccl25等。本研究与另一项转录组学分析研究筛选出的KEGG通路均包含细胞因子-细胞因子受体相互作用通路、IL-17信号通路、趋化因子信号通路[27]，且这些通路均与免疫调控相关；该研究筛选出的关键差异基因Ccl2、Ccl7与本研究筛选出的关键差异基因Ccl25属于同一家族[27]，且Ccl2、Ccl7和Ccl25在肿瘤的发生和进展中起着重要作用[28]，进一步表明NMN在缓解染尘小鼠肺损伤中的作用。综上，推测NMN可以通过免疫调节来缓解SiO2染尘小鼠的肺损伤。
本研究结果提示NMN可改善SiO2染尘诱导的肺损伤，表明NMN可能是一种辅助缓解矽肺的营养补充制剂，为矽肺的辅助治疗提供了一种新的选择和线索，但仍存在一定缺陷。首先，仅利用小鼠进行转录组测序，无法完全外推矽肺人群使用NMN的实际效果。其次，本研究设计仅为初步分析研究，鉴于机体以及矽肺病理的复杂性，其潜在分子机制以及在矽肺治疗中的预后影响需结合分子实验和临床研究进行进一步的验证，未来还需要更多实践来促进NMN的临床转化。
基金
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  • 国家自然科学基金(U22A20359)
  • 国家自然科学基金(U23A20495)
  • 四川省科技厅自然科学基金(2023NSFSC1729)
  • 四川省科技厅自然科学基金(2023NSFSC0649)
文献
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doi: 10.20043/j.cnki.MPM.202411196
  • 接收时间：2024-11-10
  • 首发时间：2026-03-17
  • 出版时间：2025-04-25
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  • 收稿日期：2024-11-10
基金
国家自然科学基金(U22A20359)
国家自然科学基金(U23A20495)
四川省科技厅自然科学基金(2023NSFSC1729)
四川省科技厅自然科学基金(2023NSFSC0649)
作者信息
    1.四川大学华西公共卫生学院/华西第四医院，卫生毒理与病理学系，四川　成都　610041
    2.四川大学华西公共卫生学院/华西第四医院，尘肺科/呼吸与危重症医学科
    3.四川大学华西公共卫生学院/华西第四医院，劳动卫生与环境卫生学系
    4.四川大学华西医院，生物治疗国家重点实验室
    5.成都川宇健维生物科技有限公司
    6.四川大学华西公共卫生学院/华西第四医院，重大疾病医防融合研究所

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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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