Bone Marrow-Derived C-Kit+ Cells Improved Inflammatory IL-33/ST-2/ILC2 Axis in the Lung Tissue of Type 2 Diabetic Rats

Inflammation is an essential factor in pulmonary complications of diabetes. Bone marrow (BM)-derived C-kit + cells have immunomodulatory properties and their transplantation is suggested as a promising strategy for ameliorating diabetes complications. This study evaluated the effect of BM-derived C-...

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Veröffentlicht in:Applied biochemistry and biotechnology 2024-10, Vol.196 (10), p.7074-7088
Hauptverfasser: Mohammadzadeh, Milad, Athari, Seyed Zanyar, Ghiasi, Fariba, Keyhanmanesh, Rana, Ghaffari-Nasab, Arshad, Roshangar, Leila, Korjan, Elnaz Salmani, Delkhosh, Aref, Bavil, Fariba Mirzaei
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Sprache:eng
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Zusammenfassung:Inflammation is an essential factor in pulmonary complications of diabetes. Bone marrow (BM)-derived C-kit + cells have immunomodulatory properties and their transplantation is suggested as a promising strategy for ameliorating diabetes complications. This study evaluated the effect of BM-derived C-kit + cells on the inflammation signaling pathway in lung tissue of type 2 diabetic male rats. Ten rats were used to extract C-kit cells, and 48 male Wistar rats weighing 180 ± 20 g were randomly divided into four equal groups: (1) Control (Cont), (2) Diabetic (D), (3) Diabetic + C-kit + cells (D + C-kit pos) intravenously injected 50-µl phosphate buffer saline (PBS) containing 300,000 C-kit + cells, and (4) Diabetic + C-kit − cells (D + C-kit neg), intravenously injected C-kit − cells. Diabetes induction increased IL-33, ST-2, CD127, and IL-2 levels and decreased IL-10. C-kit + cell therapy significantly decreased IL-33 and CD127 and increased IL-10. In addition, lung histopathological changes significantly improved in the C-kit + group compared to the diabetic group. These findings suggest that C-kit + cells may have a potential therapeutic role in mitigating diabetes-induced respiratory complications via ameliorating the inflammation and histopathological changes in lung tissue.
ISSN:0273-2289
1559-0291
1559-0291
DOI:10.1007/s12010-024-04870-1