Article(id=1200024242159973306, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1515.2022.0630, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1626019200000, receivedDateStr=2021-07-12, revisedDate=null, revisedDateStr=null, acceptedDate=1637856000000, acceptedDateStr=2021-11-26, onlineDate=1764037674703, onlineDateStr=2025-11-25, pubDate=1695830400000, pubDateStr=2023-09-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764037674703, onlineIssueDateStr=2025-11-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764037674703, creator=13701087609, updateTime=1764037674703, updator=13701087609, issue=Issue{id=1200024241572770746, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='9', pageStart='993', pageEnd='1112', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764037674563, creator=13701087609, updateTime=1764038723302, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1200028640353288193, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1200028640353288194, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1200024241572770746, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1017, endPage=1022, ext={EN=ArticleExt(id=1200024243363738556, articleId=1200024242159973306, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=The influence of exosomal miR-155 derived from monocytes stimulated by heat stress on the inflammatory response of hepatocytes, columnId=1190310110212751762, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Basic Research, runingTitle=null, highlight=null, articleAbstract=

Objective To observe the influence of exosomal miR-155 derived from monocytes stimulated by heat stress on the inflammatory response of hepatocytes. Methods According to different treatments, we termed THP-1 monocytes into the control group, the heat stress group, and the ulinasatin group. We then extracted the exosomes from each group. To study the function of exsome on hepatocytes, we incubated hepatocytes with these exosomes. We then tested the alanine aminotransferase and lactate dehydrogenase levels in the supernatant, measured cell viability, and detected the relative mRNA levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the hepatocytes. Then, the expression changes of exosomal miR-155 derived from monocytes were detected using RT-qPCR. Furthermore, the potential target of miR-155 was analyzed using database retrieval, dual-luciferase report, and Western blotting assay. Finally, the effect of monocyte exosomes on hepatocyte miR-155 and the treatment with ulinastatin or miR-155 inhibitor on hepatocyte injury were observed. Results When incubating hepatocytes with the exosomes derived from monocytes stimulated by heat stress, the levels of alanine aminotransferase and lactate dehydrogenase in the supernatant and the mRNA levels of TNF-α and IL-6 in hepatocytes were all significantly increased (P<0.01) with decreased cell survival rate (P<0.05). Heat stress increased the level of miR-155 contained in monocytes and their release of exosomes. Database retrieval, dual-luciferase reports, and Western blotting assay showed that miR-155 might target SOCS1. The exosomes from monocytes stimulated by heat stress increased miR-155 in liver cells. Ulinastatin or miR-155 inhibitor could reduce the exosomal miR-155 level and decrease TNF-α and IL-6 mRNA expression in liver cells. The difference was statistically significant (P<0.05). Conclusion The monocytes stimulated by heat stress increase the inflammatory response of hepatocytes, which may be associated with increased exosomal miR-155 using SOCS1 as a potential target. Ulinastatin may relieve the hepatocytic mRNA expression of inflammatory cytokines in this setting.

, correspAuthors=Hua-Sheng Tong, authorNote=null, correspAuthorsNote=, 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=Ming Zhang, Yue Li, Jing-Wen Yang, Xue-Zhi Shi, Ji-Biao Xiao, Hua-Sheng Tong), CN=ArticleExt(id=1200024244391343057, articleId=1200024242159973306, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=热打击单核细胞来源外泌体中miR-155对肝细胞炎症的影响及其机制, columnId=1190310110472798614, journalTitle=解放军医学杂志, columnName=基础研究, runingTitle=null, highlight=null, articleAbstract=

目的 研究热打击单核细胞来源外泌体对肝细胞炎症损伤的影响及其与外泌体miR-155的关系。方法 将单核细胞THP-1分为对照组、热打击组、乌司他丁组，分别提取3组细胞的外泌体，将其孵育肝细胞系HepG2细胞后，检测肝细胞上清中谷丙转氨酶(ALT)、乳酸脱氢酶(LDH)水平，肝细胞存活率，以及肝细胞肿瘤坏死因子-α(TNF-α)与白细胞介素-6(IL-6) mRNA水平，评估外泌体对肝细胞的作用；采用RT-qPCR检测单核细胞来源外泌体中miR-155含量的变化；通过数据库检索、双重荧光素酶报告基因检测及Western blotting实验分析miR-155的潜在靶点；观察热打击单核细胞外泌体对肝细胞miR-155的影响，以及使用乌司他丁或miR-155抑制剂处理对这些外泌体功能的影响。结果 热打击单核细胞来源外泌体使肝细胞上清ALT及LDH水平、TNF-α mRNA及IL-6 mRNA水平明显增高(P<0.01)，细胞存活率下降(P<0.05)；热打击能增加单核细胞及其释放外泌体内含的miR-155水平；miR-155可能以细胞因子信号传导抑制分子1(SOCS1)作为靶基因发挥作用；采用热打击单核细胞外泌体孵育肝细胞可使后者miR-155水平增高，乌司他丁或miR-155抑制剂能降低热打击单核细胞外泌体miR-155水平并减少肝细胞TNF-α和IL-6 mRNA的表达，差异有统计学意义(P<0.05)。结论 热打击单核细胞可上调肝细胞炎性因子导致的炎症损伤，这可能是通过释放外泌体miR-155至肝细胞并以SOCS1为潜在靶点实现的；乌司他丁可能缓解此条件下肝细胞内炎性因子mRNA的表达。

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ALT. 谷丙转氨酶；LDH. 乳酸脱氢酶；与对照组比较，(1)P<0.05；与热打击组比较，(2)P<0.05

, figureFileSmall=ACV+ZbV0yPOy2UqOnWnf1A==, figureFileBig=8jSkQsM2coH2kGhaFUHdCw==, tableContent=null), ArticleFig(id=1200066180909200210, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=EN, label=Fig.2, caption=The expression of miR-155 in the monocytes and the exosome derived from monocytes, figureFileSmall=Lc96C7/UFl4OphGiWR5e5Q==, figureFileBig=VvkUnEYTSOo2AP66HvpRuw==, tableContent=null), ArticleFig(id=1200066180976309077, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=CN, label=图2, caption=单核细胞及其来源外泌体内miR-155水平

与对照组比较，(1)P<0.05；与热打击组比较，(2)P<0.05

, figureFileSmall=Lc96C7/UFl4OphGiWR5e5Q==, figureFileBig=VvkUnEYTSOo2AP66HvpRuw==, tableContent=null), ArticleFig(id=1200066181064389464, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=EN, label=Fig.3, caption=miR-155 regulates the inflammatory damage of liver cells in a SOCS1-dependent manner, figureFileSmall=NbwhEfqiSdZ3Q2Coo7tLmQ==, figureFileBig=BDlrN3zYtJhWejfoVFT8rQ==, tableContent=null), ArticleFig(id=1200066181135692636, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=CN, label=图3, caption=miR-155通过靶向SOCS1调控肝脏炎症反应

A. 生物信息学工具预测SOCS1是miR-155的靶基因；B. 双重荧光素酶报告实验检测miR-155模拟物对SOCS1基因转录水平的影响，与miR对照组比较，(1)P<0.05；C. Western blotting检测各组外泌体对肝细胞内SOCS1、p-NF-κB蛋白表达的影响，与对照组比较，(1)P<0.05；与热打击组比较，(2)P<0.05；D. RT-PCR检测转染miR-155抑制物及siSOCS1后热打击肝细胞的炎性因子水平，(1)P<0.05

, figureFileSmall=NbwhEfqiSdZ3Q2Coo7tLmQ==, figureFileBig=BDlrN3zYtJhWejfoVFT8rQ==, tableContent=null), ArticleFig(id=1200066181223773023, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=EN, label=Fig. 4, caption=The monocytes stimulated by heat stress affect hepatocyte inflammation by exosome containing miR-155, figureFileSmall=5l5+4JwFuhamBkXqhLDKUg==, figureFileBig=KRlswMHatAOClHbm3TJGPg==, tableContent=null), ArticleFig(id=1200066181320242018, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=CN, label=图4, caption=热打击单核细胞通过内含miR-155影响肝细胞炎症反应

A. 经各组单核细胞来源外泌体处理的肝细胞内miR-155表达水平；与对照组比较，(1)P<0.05；与热打击组比较，(2)P<0.05。B. 转染了阴性对照和miR-155抑制剂的热打击单核细胞来源外泌体作用于肝细胞。C. 热打击单核细胞来源外泌体处理转染了阴性对照和miR-155的肝细胞。D. 热打击单核细胞来源外泌体处理转染了阴性对照和miR-155模拟剂的肝细胞。所有实验独立重复3次。与阴性对照比较，(1)P<0.05

, figureFileSmall=5l5+4JwFuhamBkXqhLDKUg==, figureFileBig=KRlswMHatAOClHbm3TJGPg==, tableContent=null), ArticleFig(id=1200066181429293925, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=EN, label=Tab.1, caption=

The primer sequences in the study

, figureFileSmall=null, figureFileBig=null, tableContent=

基因	引物序列(5'→3')
miR-155	正向：GGGGTAATGCTAATCGTGA
	反向：CAGTGCGTGTCGTGGAG
TNF-α	正向：CTTCTCATTCCTGCTTGTG
	反向：ACTTGGTGGTTTGCTACG
IL-6	正向：GGCGGATCGGATGTTGTGAT
	反向：GGACCCCAGACAATCGGTTG
GAPDH	正向：CAATGTGTCCGTCGTGGATCT
	反向：GTCCTCAGTGTAGCCCAAGATG
U6	正向：CGAGCACAGAATCGCTTCA
	反向：CTCGCTTCGGCAGCACATAT

), ArticleFig(id=1200066181521568614, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1200024242159973306, language=CN, label=表1, caption=

基因引物序列

, figureFileSmall=null, figureFileBig=null, tableContent=

基因	引物序列(5'→3')
miR-155	正向：GGGGTAATGCTAATCGTGA
	反向：CAGTGCGTGTCGTGGAG
TNF-α	正向：CTTCTCATTCCTGCTTGTG
	反向：ACTTGGTGGTTTGCTACG
IL-6	正向：GGCGGATCGGATGTTGTGAT
	反向：GGACCCCAGACAATCGGTTG
GAPDH	正向：CAATGTGTCCGTCGTGGATCT
	反向：GTCCTCAGTGTAGCCCAAGATG
U6	正向：CGAGCACAGAATCGCTTCA
	反向：CTCGCTTCGGCAGCACATAT

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