{"title":"miRNA-301是通过诱导炎症促进坏死性小肠结肠炎的分子。","authors":"Dajun Zou, Fude Hu, Qili Zhou, Xiaoqing Xu","doi":"10.18388/abp.2020_6806","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Necrotizing enterocolitis (NEC) is a devastating inflammatory disease with high morbidity and mortality, mainly affecting premature infants. This study aimed to explore the role of miRNA-301a in the pathogenesis of NEC.</p><p><strong>Methods: </strong>The differentially expressed miRNAs and mRNAs were screened by collating RNA-Seq data from the GEO database of intestinal tissue samples. The differential miRNA-mRNAs regulatory network was constructed based on functional enrichment analysis. Newborn BALB/c mice were used to establish the NEC model. Haematoxylin and eosin staining was used to assess intestinal damage. The levels of IL-8 and TNF-α in mouse serum were evaluated by ELISA. qRT-PCR was used to detect the expression of miRNA-301a in intestinal tissues.</p><p><strong>Results: </strong>Bioinformatics analysis showed that miRNA-301a was involved in intestinal lesions. Intestinal tissue damage was reduced and serum levels of the inflammatory cytokines IL-8 and TNF-α were lower in NEC model mice treated with miRNA-301a antagonists. The level of miRNA-301a in intestinal tissues of NEC model mice was significantly higher than in the control group and miRNA-301a antagonists treated group.</p><p><strong>Conclusion: </strong>miRNA-301a plays an important role in the pathogenesis of NEC by promoting inflammation, and is a potential therapeutic target of NEC.</p>","PeriodicalId":6984,"journal":{"name":"Acta biochimica Polonica","volume":" ","pages":"905-910"},"PeriodicalIF":1.4000,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"miRNA-301 As a molecule promoting necrotizing enterocolitis by inducing inflammation.\",\"authors\":\"Dajun Zou, Fude Hu, Qili Zhou, Xiaoqing Xu\",\"doi\":\"10.18388/abp.2020_6806\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Necrotizing enterocolitis (NEC) is a devastating inflammatory disease with high morbidity and mortality, mainly affecting premature infants. This study aimed to explore the role of miRNA-301a in the pathogenesis of NEC.</p><p><strong>Methods: </strong>The differentially expressed miRNAs and mRNAs were screened by collating RNA-Seq data from the GEO database of intestinal tissue samples. The differential miRNA-mRNAs regulatory network was constructed based on functional enrichment analysis. Newborn BALB/c mice were used to establish the NEC model. Haematoxylin and eosin staining was used to assess intestinal damage. The levels of IL-8 and TNF-α in mouse serum were evaluated by ELISA. qRT-PCR was used to detect the expression of miRNA-301a in intestinal tissues.</p><p><strong>Results: </strong>Bioinformatics analysis showed that miRNA-301a was involved in intestinal lesions. Intestinal tissue damage was reduced and serum levels of the inflammatory cytokines IL-8 and TNF-α were lower in NEC model mice treated with miRNA-301a antagonists. The level of miRNA-301a in intestinal tissues of NEC model mice was significantly higher than in the control group and miRNA-301a antagonists treated group.</p><p><strong>Conclusion: </strong>miRNA-301a plays an important role in the pathogenesis of NEC by promoting inflammation, and is a potential therapeutic target of NEC.</p>\",\"PeriodicalId\":6984,\"journal\":{\"name\":\"Acta biochimica Polonica\",\"volume\":\" \",\"pages\":\"905-910\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2023-11-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta biochimica Polonica\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.18388/abp.2020_6806\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta biochimica Polonica","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.18388/abp.2020_6806","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
miRNA-301 As a molecule promoting necrotizing enterocolitis by inducing inflammation.
Objective: Necrotizing enterocolitis (NEC) is a devastating inflammatory disease with high morbidity and mortality, mainly affecting premature infants. This study aimed to explore the role of miRNA-301a in the pathogenesis of NEC.
Methods: The differentially expressed miRNAs and mRNAs were screened by collating RNA-Seq data from the GEO database of intestinal tissue samples. The differential miRNA-mRNAs regulatory network was constructed based on functional enrichment analysis. Newborn BALB/c mice were used to establish the NEC model. Haematoxylin and eosin staining was used to assess intestinal damage. The levels of IL-8 and TNF-α in mouse serum were evaluated by ELISA. qRT-PCR was used to detect the expression of miRNA-301a in intestinal tissues.
Results: Bioinformatics analysis showed that miRNA-301a was involved in intestinal lesions. Intestinal tissue damage was reduced and serum levels of the inflammatory cytokines IL-8 and TNF-α were lower in NEC model mice treated with miRNA-301a antagonists. The level of miRNA-301a in intestinal tissues of NEC model mice was significantly higher than in the control group and miRNA-301a antagonists treated group.
Conclusion: miRNA-301a plays an important role in the pathogenesis of NEC by promoting inflammation, and is a potential therapeutic target of NEC.
期刊介绍:
Acta Biochimica Polonica is a journal covering enzymology and metabolism, membranes and bioenergetics, gene structure and expression, protein, nucleic acid and carbohydrate structure and metabolism.