Hypoxic MSCs Secretome Modulates IL-18-Mediated Inflammatory in Type 2 Diabetes Mellitus via AP-1 Regulation

Authors

  • Fajar Amansyah Department of Postgraduate Medical Science, Faculty of Medicine, Hasanuddin University, Kota Makassar, Sulawesi Selatan 90245, Indonesia
  • Iffan Alif Stem Cell and Cancer Research (SCCR), Faculty of Medicine, Sultan Agung Islamic University (UNISSULA), Semarang, Indonesia
  • Risky Candra Satria Irawan Postgraduate student of Biomedical Science, Medical Faculty, Sultan Agung Islamic University (UNISSULA), Semarang, Central Java, Indonesia
  • Haerani Rasyid Department of Internal Medicine, Faculty of Medicine, Hasanuddin University, Makassar, South Sulawesi, 90245, Indonesia

DOI:

https://doi.org/10.59278/cbs.v3i7.47

Keywords:

AP-1, Hypoxic MSCs, IL-18, Secretome, T2DM

Abstract

Background: Chronic inflammation is central to the pathophysiology of Type 2 Diabetes Mellitus (T2DM), contributing to the progression of metabolic dysfunction characterized by hyperglycaemia and insulin resistance. This study aims to investigate the therapeutic potential of the hypoxic MSCs secretome (SH-MSCs) in reducing inflammation of a T2DM rat model. Methods: T2DM was induced in Wistar rats through a high-fat diet (HFD) followed by streptozotocin (STZ) administration. A total of 24 healthy male Wistar rats were randomly assigned to five groups: healthy control, T2DM, T2DM + metformin, T2DM + SH-MSCs. Results: SH-MSCs significantly reduced IL-18 mRNA expression, a key indicator of proinflammation, and suppressed the expression of AP-1 mRNA, a crucial proinflammatory transcription factor. Conclusion: These findings highlight the therapeutic potential of SH-MSCs as an alternative approach to alleviate inflammation in T2DM.

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Published

2025-04-26

Issue

Vol. 3 No. 7 (2024)

Section

Articles

How to Cite

Hypoxic MSCs Secretome Modulates IL-18-Mediated Inflammatory in Type 2 Diabetes Mellitus via AP-1 Regulation. (2025). International Journal of Cell and Biomedical Science, 3(7), 189-200. https://doi.org/10.59278/cbs.v3i7.47

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