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Ischemia reperfusion injury (IRI) is the major cause of intestinal damage in clinic. Although either mesenchymal stromal cells (MSCs) or interleukin 37 (IL-37) shows some beneficial roles to ameliorate IRI, their effects are limited. In this study, the preventative effects of IL-37 gene-modified MSCs (IL-37-MSCs) on intestinal IRI are investigated.\n                    <jats:italic>Methods<\/jats:italic>\n                    . Intestinal IRI model was established by occluding the superior mesenteric artery for 30 minutes and then reperfused for 72 hours in rats. Forty adult male Sprague-Dawley rats were randomly divided into the sham control, IL-37-MSC-treated, MSC-treated, recombinant IL-37- (rIL-37-) treated, and untreated groups. Intestinal damage was assessed by H&amp;E staining. The levels of gut barrier function factors (diamine oxidase and D-Lactate) and inflammation cytokine IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    were assayed using ELISA. The synthesis of tissue damage-related NLRP3 inflammasome and downstream cascade reactions including cleaved caspase-1, IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , and IL-18 was detected by western blot. The mRNA levels of proinflammatory mediators IL-6 and TNF-\n                    <jats:italic>\u03b1<\/jats:italic>\n                    , which are downstream of IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    and IL-18, were determined by qPCR. Data were analyzed by one-way analysis of variance (ANOVA) after the normality test and followed by post hoc analysis with the least significant difference (LSD) test.\n                    <jats:italic>Results<\/jats:italic>\n                    . IL-37-MSCs were able to migrate to the damaged tissue and significantly inhibit intestinal IRI. As compared with MSCs or the rIL-37 monotherapy group, IL-37-MSC treatment both improved gut barrier function and decreased local and systemic inflammation cytokine IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    level in IRI rats. In addition, tissue damage-related NLRP3 and downstream targets (cleaved caspase-1, IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , and IL-18) were significantly decreased in IRI rats treated with IL-37-MSCs. Furthermore, IL-1\n                    <jats:italic>\u03b2<\/jats:italic>\n                    - and IL-18-related proinflammatory mediator IL-6 and TNF-\n                    <jats:italic>\u03b1<\/jats:italic>\n                    mRNA expressions were all significantly decreased in IRI rats treated with IL-37-MSCs.\n                    <jats:italic>Conclusion<\/jats:italic>\n                    . The results suggest that IL-37 gene modification significantly enhances the protective effects of MSCs against intestinal IRI. In addition, NLRP3-related signaling pathways could be associated with IL-37-MSC-mediated protection.\n                  <\/jats:p>","DOI":"10.1155\/2020\/8883636","type":"journal-article","created":{"date-parts":[[2020,8,8]],"date-time":"2020-08-08T19:32:22Z","timestamp":1596915142000},"page":"1-12","source":"Crossref","is-referenced-by-count":13,"title":["IL-37 Gene Modification Enhances the Protective Effects of Mesenchymal Stromal Cells on Intestinal Ischemia Reperfusion Injury"],"prefix":"10.1155","volume":"2020","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6878-9293","authenticated-orcid":true,"given":"Dejun","family":"Kong","sequence":"first","affiliation":[{"name":"Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, China"},{"name":"Tianjin General Surgery Institute, Tianjin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yonghao","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of General 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