Iranian Journal of Basic Medical Sciences، جلد ۲۳، شماره ۶، صفحات ۷۵۱-۷۵۹

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عنوان انگلیسی Simvastatin combined with bone marrow mesenchymal stromal cells (BMSCs) improve burn wound healing by ameliorating angiogenesis through SDF-1α/CXCR4 pathway
چکیده انگلیسی مقاله Objective(s): Chemokines are wound mediators that promote angiogenesis during wound healing. We hypothesized that Simvastatin in combination with the bone marrow mesenchymal stromal cells (BMSCs) improve burn wound healing by ameliorating angiogenesis via SDF-1α/CXCR4 pathway.Materials and Methods: Under general anesthesia, deep partial-thickness burns were created on the inter-scapular area of 48 male rats. Study groups were administrated with petroleum jelly (Simvastatin Vehicle), a single dose of intradermal BMSCs (1×106), topical Simvastatin (0.5 mg/kg) daily and combination of BMSCs and Simvastatin for 14 days. In this study, we used MTT assay, in vivo and in vitro wound closure, H&E and Trichorome staining, immunohistochemistry (IHC), real- time PCR, Western blot and tube formation assay.Results: A significant improvement in wound closure percentage, epithelial thickness, collagen remodeling, and up-regulation of stromal cell-derived factor 1 alpha (SDF1α), C-X-C chemokine receptor type 4 (CXCR4), protein kinase B (AKT), and phosphatidylinositol 3- kinase (PI3K), as well as CD31 and vascular endothelial growth factor (VEGF) expression were observed after treatment with simvastatin, BMSCs and combination of them compared to the vehicle group. However, the co-treatment group revealed considerable superiority in examined factors. BMSCs treated with Simvastatin showed the highest viability in the concentration of 0.5 and 1 Nanomolar (nM). Increment in proliferation and capillary vessels formation of BMSCs was observed in the 0.5 nM and 1 nM concentrations of Simvastatin in vitro. Conclusion: Treatment of deep partial-thickness of burns with co-treatment of BMSCs and Simvastatin resulted in improved burn wound healing through up-regulating of SDF-1α/CXCR4 pathway.
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نویسندگان مقاله | Javad Mohajer Ansari
Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Parisa Ramhormozi
Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Ronak Shabani
Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Hamidreza Pazoki-toroudi
Physiology research center and department of physiology, faculty of medicine, Iran University of Medical Sciences, Tehran, Iran


| Abazar Yari
Department of Anatomy, faculty of medicine, Alborz University of Medical Sciences, Karaj, Iran|Dietary Supplements and Probiotics Research Center, Alborz University of Medical Sciences, Karaj, Iran


| Mahmood Barati
Deparment of medical biotechnology, faculty of allied medicine, Iran University of Medical Sciences, Tehran, Iran


| Mostafa Dahmardehei
Burn research center, Iran University of Medical Sciences, Tehran, Iran


| Azar Babakhani
Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Maliheh Nobakht
Department of Anatomical Sciences, School of Medicine, Iran University of Medical Sciences, Tehran, Iran|Anti-Microbial Resistance Research Center, Iran University of Medical Sciences, Tehran, Iran



نشانی اینترنتی http://ijbms.mums.ac.ir/article_15506.html
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زبان مقاله منتشر شده en
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نوع مقاله منتشر شده Original Article
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