Anti-inflammatory effect of UC-MSC secretome on diabetic ulcer model rats: Study of Ccl22 and Cxcl12 mRNA expression
A K Prambodo1, D A A Nugrahaningsih2, S M Haryana3
1Magister of Biotechnology, Faculty of Postgraduate, Universitas Gadjah Mada, Yogyakarta, DI Yogyakarta, Indonesia.
Introduction:
Diabetes mellitus is a metabolic disorder which is characterized by chronic hyperglycemia condition and this condition can cause some complications such as diabetic ulcers. Secretome from UC-MSC is an alternative treatment that being developed for accelerating wound healing of diabetic ulcers. The aim of this research is to study the effect of UC-MSC secretome for wound healing of diabetic ulcers in Nicotinamide-Streptozotocin (NA-STZ) induced Wistar rats and the mechanism through mRNA CCL22 and CXCL12 expression study.
Materials And Methods:
Fifteen male Wistar rats were divided into the diabetes group and the normal group. The diabetes group consists of the diabetes control group given by 0.02 ml MEM-α, the secretome group 0.004 ml, the secretome group 0.02 ml, and the secretome group 0.4 ml, and the normal group. Wounds are created on the back of the hyperglycemia rats and given the treatment intradermally. Wounded skin was collected for RNA extraction. RNA total yield used for cDNA synthesis. cDNA used as a template for Polymerase Chain Reaction (PCR) and using Agarose electrophoresis to view mRNA CCL22 and CXCL12 expression. Gene expression was normalized using mRNA GAPDH. Online software Targetscan and miRTarbase are used for selection of miRNA which have potentially targeted CCL22 and CXCL12 mRNA.
Results:
NA-STZ affect increasing blood glucose. Injection of 0.02 ml UC-MSC secretome showed a better impact on wound healing than the diabetes control group. Lower expression of mRNA CCL22 and CXCL12 showed in male Wistar rats induced NA-STZ with UC-MSC secretome treatments.
Conclusion:
UC-MSC secretomes have potential therapy as anti-ulcer on hyperglycemia male Wistar rats induced NASTZ with probability via hsa-23a-3p in nuclear factor-kappa β (NF-κβ) pathway via inflammation mechanism.
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