| Autor: |
Jameel Al-Tamimi, Ibrahim M. Alhazza, Hossam Ebaid, Iftekhar Hassan, Sufia Husain, Saleh Alwasel, Ashraf Mashaly |
| Jazyk: |
angličtina |
| Rok vydání: |
2024 |
| Předmět: |
|
| Zdroj: |
Journal of King Saud University: Science, Vol 36, Iss 3, Pp 103088- (2024) |
| Druh dokumentu: |
article |
| ISSN: |
1018-3647 |
| DOI: |
10.1016/j.jksus.2023.103088 |
| Popis: |
Diabetes Mellitus during wound healing alters macrophage recruitment, leading to delayed healing. The present study focuses on impact of camel milk peptide (CMP) on macrophage plasticity during their recruitment during wound healing stages. The Swiss albino rats were distributed into three groups: a normal wounded group (control), a wounded diabetic group, and a wounded diabetic group treated with CMP daily. The diabetic rats showed a significantly compromised level of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein (MIP-1α) relative gene expression, anti-CD31, anti-Mac-3, and anti-CD68 staining than the control group. Macrophages were considerably depleted in diabetic group animals upon initiating the inflammatory phase, while the protein significantly reversed the same. Also, there was marked increase in pathogenic bacterial growth at the wound sites of diabetic rats. On the contrary, in CMP-diabetic rats, levels of pathogenic bacteria were comparable to normal control animals. Diabetic rats demonstrated a reduction in matrix metalloproteinase (MMP-9 and MMP-13) expression while increased TNF-α levels compared to control rats. In addition, they also showed significantly reduced expression of VEGF and fibroblast growth factors (FGF) genes and IL-10 during the proliferation phase. However, all these parameters exhibited a considerably reversed trend in the CMP treated diabetic rats. Hence, CMP-treated diabetic rats demonstrated a transition to the M2 phenotype, highlighting macrophage recruitment's critical role in healing of wounds in hyperglycemic rats. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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