Li-Lan Huang, Ji Yang, Yue-Yuan Hou, Yi-Hua Bai, Hong-Ying Jiang
{"title":"骨髓间充质干细胞通过调节炎症因子IL-11改善糖尿病和糖尿病肾纤维化。","authors":"Li-Lan Huang, Ji Yang, Yue-Yuan Hou, Yi-Hua Bai, Hong-Ying Jiang","doi":"10.2174/011574888X348254241216171655","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the therapeutic potential of mesenchymal stem cells (MSC) in treating diabetic nephropathy (DN) by investigating their effect on IL-11 modulation in a mouse model.</p><p><strong>Methods: </strong>The effects of MSC therapy on DN were examined both in vivo and in vitro. Sixty adult male C57BL/6 mice were divided into the streptozotocin (STZ) diabetes (T1D) and the high-fat diet diabetes (T2D) models, with both groups receiving MSC treatment or saline for 4 or 8 weeks. Blood glucose, serum urea, interleukin-11 (IL-11), and kidney fibrosis markers were measured. Additionally, western blotting was used to assess levels of Type I and III collagen, E-Cadherin, α- smooth muscle actin (α-SMA), Vimentin, and ferroptosis suppressor protein 1 (FSP-1).</p><p><strong>Results: </strong>MSC-treated T1D and T2D mice showed reduced blood glucose, serum urea, IL-11, TGF-β, and fibrosis markers (type I and III collagen, α-SMA, Vimentin, FSP-1), alongside increased E-Cadherin expression. Similar effects were observed in vitro using mouse glomerular epithelial cells, confirming MSC-mediated suppression of fibrosis pathways.</p><p><strong>Conclusion: </strong>MSC therapy improves nephropathy, likely by inhibiting IL-11 and reducing fibrosis- related markers, making it a promising treatment for DN.</p>","PeriodicalId":93971,"journal":{"name":"Current stem cell research & therapy","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bone Marrow Mesenchymal Stem Cells Ameliorate Diabetes and Diabetic Renal Fibrosis by Modulating the Inflammatory Factor IL-11.\",\"authors\":\"Li-Lan Huang, Ji Yang, Yue-Yuan Hou, Yi-Hua Bai, Hong-Ying Jiang\",\"doi\":\"10.2174/011574888X348254241216171655\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>This study aims to explore the therapeutic potential of mesenchymal stem cells (MSC) in treating diabetic nephropathy (DN) by investigating their effect on IL-11 modulation in a mouse model.</p><p><strong>Methods: </strong>The effects of MSC therapy on DN were examined both in vivo and in vitro. Sixty adult male C57BL/6 mice were divided into the streptozotocin (STZ) diabetes (T1D) and the high-fat diet diabetes (T2D) models, with both groups receiving MSC treatment or saline for 4 or 8 weeks. Blood glucose, serum urea, interleukin-11 (IL-11), and kidney fibrosis markers were measured. Additionally, western blotting was used to assess levels of Type I and III collagen, E-Cadherin, α- smooth muscle actin (α-SMA), Vimentin, and ferroptosis suppressor protein 1 (FSP-1).</p><p><strong>Results: </strong>MSC-treated T1D and T2D mice showed reduced blood glucose, serum urea, IL-11, TGF-β, and fibrosis markers (type I and III collagen, α-SMA, Vimentin, FSP-1), alongside increased E-Cadherin expression. Similar effects were observed in vitro using mouse glomerular epithelial cells, confirming MSC-mediated suppression of fibrosis pathways.</p><p><strong>Conclusion: </strong>MSC therapy improves nephropathy, likely by inhibiting IL-11 and reducing fibrosis- related markers, making it a promising treatment for DN.</p>\",\"PeriodicalId\":93971,\"journal\":{\"name\":\"Current stem cell research & therapy\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-12-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current stem cell research & therapy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/011574888X348254241216171655\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current stem cell research & therapy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/011574888X348254241216171655","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Bone Marrow Mesenchymal Stem Cells Ameliorate Diabetes and Diabetic Renal Fibrosis by Modulating the Inflammatory Factor IL-11.
Objective: This study aims to explore the therapeutic potential of mesenchymal stem cells (MSC) in treating diabetic nephropathy (DN) by investigating their effect on IL-11 modulation in a mouse model.
Methods: The effects of MSC therapy on DN were examined both in vivo and in vitro. Sixty adult male C57BL/6 mice were divided into the streptozotocin (STZ) diabetes (T1D) and the high-fat diet diabetes (T2D) models, with both groups receiving MSC treatment or saline for 4 or 8 weeks. Blood glucose, serum urea, interleukin-11 (IL-11), and kidney fibrosis markers were measured. Additionally, western blotting was used to assess levels of Type I and III collagen, E-Cadherin, α- smooth muscle actin (α-SMA), Vimentin, and ferroptosis suppressor protein 1 (FSP-1).
Results: MSC-treated T1D and T2D mice showed reduced blood glucose, serum urea, IL-11, TGF-β, and fibrosis markers (type I and III collagen, α-SMA, Vimentin, FSP-1), alongside increased E-Cadherin expression. Similar effects were observed in vitro using mouse glomerular epithelial cells, confirming MSC-mediated suppression of fibrosis pathways.
Conclusion: MSC therapy improves nephropathy, likely by inhibiting IL-11 and reducing fibrosis- related markers, making it a promising treatment for DN.
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