Notoginsenoside R1 Facilitated Wound Healing in High-Fat Diet/Streptozotocin-Induced Diabetic Rats
Diabetic ulcers bring about high morbidity and mortality in patients and cause a great economic burden to society as a whole. Since existing treatments cannot fulfil patient requirements, it is urgent to find effective therapies. In this study, the wound healing effect of topical notoginsenoside R1...
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| creator | Cao, Guangzhao Xiang, Changpei Zhou, Rui Zhang, Yi Xu, He Yang, Hongjun Zhang, Jingjing |
| description | Diabetic ulcers bring about high morbidity and mortality in patients and cause a great economic burden to society as a whole. Since existing treatments cannot fulfil patient requirements, it is urgent to find effective therapies. In this study, the wound healing effect of topical notoginsenoside R1 (NR1) treatment on diabetic full-thickness wounds in type II diabetes mellitus (T2DM) was induced by the combination of a high-fat diet and streptozotocin (STZ) injection. NR1 significantly increased the wound closure rate, enhanced extracellular matrix (ECM) secretion, promoted collagen growth, increased platelet endothelial cell adhesion molecule-1 (CD31) expression, and decreased cleaved caspase-3 expression. RNA-Seq analysis identified ECM remodeling and inflammation as critical biological processes and Timp1 and Mmp3 as important targets in NR1-mediated wound healing. Further experiments showed that NR1-treated wounds demonstrated higher expression of tissue inhibitor of metalloproteinase 1 (TIMP1) and transforming growth factor-β1 (TGFβ1) and lower expression of matrix metallopeptidase 9 (MMP9), matrix metallopeptidase 3 (MMP3), interleukin-1β (IL-1β), and interleukin-6 (IL-6) than diabetic wounds. These investigations promote the understanding of the mechanism of NR1-mediated diabetic wound healing and provide a promising therapeutic drug to enhance diabetic wound healing. |
| doi_str_mv | 10.1155/2022/2476493 |
| format | Article |
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Since existing treatments cannot fulfil patient requirements, it is urgent to find effective therapies. In this study, the wound healing effect of topical notoginsenoside R1 (NR1) treatment on diabetic full-thickness wounds in type II diabetes mellitus (T2DM) was induced by the combination of a high-fat diet and streptozotocin (STZ) injection. NR1 significantly increased the wound closure rate, enhanced extracellular matrix (ECM) secretion, promoted collagen growth, increased platelet endothelial cell adhesion molecule-1 (CD31) expression, and decreased cleaved caspase-3 expression. RNA-Seq analysis identified ECM remodeling and inflammation as critical biological processes and Timp1 and Mmp3 as important targets in NR1-mediated wound healing. Further experiments showed that NR1-treated wounds demonstrated higher expression of tissue inhibitor of metalloproteinase 1 (TIMP1) and transforming growth factor-β1 (TGFβ1) and lower expression of matrix metallopeptidase 9 (MMP9), matrix metallopeptidase 3 (MMP3), interleukin-1β (IL-1β), and interleukin-6 (IL-6) than diabetic wounds. These investigations promote the understanding of the mechanism of NR1-mediated diabetic wound healing and provide a promising therapeutic drug to enhance diabetic wound healing.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/2476493</identifier><identifier>PMID: 35069970</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Angiogenesis ; Animals ; Antibodies ; Antioxidants ; Apoptosis ; Collagen ; Cytokines ; Debridement ; Diabetes ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetic Angiopathies - drug therapy ; Diet, High-Fat - adverse effects ; Fasting ; Ginsenosides - pharmacology ; Ginsenosides - therapeutic use ; Glucose ; Growth factors ; Humans ; Male ; Panax - chemistry ; Physiology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Software ; Streptozocin - adverse effects ; Tumor necrosis factor-TNF ; Ulcer - drug therapy ; Ulcers ; Wound healing ; Wound Healing - drug effects</subject><ispartof>Oxidative medicine and cellular longevity, 2022, Vol.2022, p.2476493-15</ispartof><rights>Copyright © 2022 Guangzhao Cao et al.</rights><rights>Copyright © 2022 Guangzhao Cao et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Guangzhao Cao et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-e36ae1aa37d98646e766d1be0cf0ec32ff4ce48b5a67d9319664477566f95cc73</citedby><cites>FETCH-LOGICAL-c514t-e36ae1aa37d98646e766d1be0cf0ec32ff4ce48b5a67d9319664477566f95cc73</cites><orcidid>0000-0001-5494-9236 ; 0000-0002-9210-9403 ; 0000-0003-1109-9248 ; 0000-0003-0039-6888 ; 0000-0001-5501-3288 ; 0000-0003-2783-0998 ; 0000-0002-1349-9184</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8777460/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8777460/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35069970$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Luis Franco, Jeferson</contributor><contributor>Jeferson Luis Franco</contributor><creatorcontrib>Cao, Guangzhao</creatorcontrib><creatorcontrib>Xiang, Changpei</creatorcontrib><creatorcontrib>Zhou, Rui</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Xu, He</creatorcontrib><creatorcontrib>Yang, Hongjun</creatorcontrib><creatorcontrib>Zhang, Jingjing</creatorcontrib><title>Notoginsenoside R1 Facilitated Wound Healing in High-Fat Diet/Streptozotocin-Induced Diabetic Rats</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Diabetic ulcers bring about high morbidity and mortality in patients and cause a great economic burden to society as a whole. Since existing treatments cannot fulfil patient requirements, it is urgent to find effective therapies. In this study, the wound healing effect of topical notoginsenoside R1 (NR1) treatment on diabetic full-thickness wounds in type II diabetes mellitus (T2DM) was induced by the combination of a high-fat diet and streptozotocin (STZ) injection. NR1 significantly increased the wound closure rate, enhanced extracellular matrix (ECM) secretion, promoted collagen growth, increased platelet endothelial cell adhesion molecule-1 (CD31) expression, and decreased cleaved caspase-3 expression. RNA-Seq analysis identified ECM remodeling and inflammation as critical biological processes and Timp1 and Mmp3 as important targets in NR1-mediated wound healing. 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Since existing treatments cannot fulfil patient requirements, it is urgent to find effective therapies. In this study, the wound healing effect of topical notoginsenoside R1 (NR1) treatment on diabetic full-thickness wounds in type II diabetes mellitus (T2DM) was induced by the combination of a high-fat diet and streptozotocin (STZ) injection. NR1 significantly increased the wound closure rate, enhanced extracellular matrix (ECM) secretion, promoted collagen growth, increased platelet endothelial cell adhesion molecule-1 (CD31) expression, and decreased cleaved caspase-3 expression. RNA-Seq analysis identified ECM remodeling and inflammation as critical biological processes and Timp1 and Mmp3 as important targets in NR1-mediated wound healing. Further experiments showed that NR1-treated wounds demonstrated higher expression of tissue inhibitor of metalloproteinase 1 (TIMP1) and transforming growth factor-β1 (TGFβ1) and lower expression of matrix metallopeptidase 9 (MMP9), matrix metallopeptidase 3 (MMP3), interleukin-1β (IL-1β), and interleukin-6 (IL-6) than diabetic wounds. 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| subjects | Angiogenesis Animals Antibodies Antioxidants Apoptosis Collagen Cytokines Debridement Diabetes Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - drug therapy Diabetic Angiopathies - drug therapy Diet, High-Fat - adverse effects Fasting Ginsenosides - pharmacology Ginsenosides - therapeutic use Glucose Growth factors Humans Male Panax - chemistry Physiology Rats Rats, Sprague-Dawley Rodents Software Streptozocin - adverse effects Tumor necrosis factor-TNF Ulcer - drug therapy Ulcers Wound healing Wound Healing - drug effects |
| title | Notoginsenoside R1 Facilitated Wound Healing in High-Fat Diet/Streptozotocin-Induced Diabetic Rats |
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