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Background <p>Small extracellular vesicles (sEVs) derived from mesenchymal stem cells are emerging as promising therapeutic agents in regenerative medicine. This study evaluated the therapeutic potential of sEVs from 3D-cultured canine adipose-derived mesenchymal stem cells in alleviating diabetes-induced systemic dysfunctions, focusing on their revitalizing, metabolic, and immunomodulatory properties.</p> Results <p>sEVs were identified as nanosized vesicles around 72&#xa0;nm with a negative zeta potential (-21.15 mV) and a high particle concentration (1.07 × 10<sup>9</sup> particles/mL). In vitro, sEVs (10<sup>4</sup> particles/mL) protected INS-1 β-cells from etoposide (ETO)-induced cytotoxicity, enhancing cell viability, reducing apoptosis, and promoting recovery. Biodistribution analysis showed detectable levels in plasma for up to 24&#xa0;h post-injection, suggesting sustained circulation and a potentially extended half-life compared to free therapeutic molecules. In streptozotocin (STZ)-induced diabetic mice, sEV treatment significantly improved glycemic control, enhanced glucose metabolism, and restored β-cell function, as reflected by improvements in HOMA-β, HOMA-IR, and QUICKI indices. Additionally, sEVs reduced systemic inflammation, restored immune homeostasis, and improved hematological, renal, and hepatic parameters. Double-dose sEV administration yielded the most pronounced therapeutic benefits, including enhanced glucose clearance and systemic recovery.</p> Conclusions <p>sEVs exhibit robust revitalizing, metabolic, and immunomodulatory properties, effectively mitigating diabetes-related dysfunctions in vitro and in vivo. These findings highlight sEVs as a novel regenerative therapy for diabetes and its complications, providing a strong foundation for future clinical translation.</p>

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Small extracellular vesicles produced from canine adipose-derived mesenchymal stem cells mitigate diabetes mellitus in streptozotocin-induced mice via β-cell revitalization

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月10日

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  • Parkpoom Siriarchavatana,
  • Saranyou Oontawee,
  • Watchareewan Rodprasert,
  • Anatcha Thongsit,
  • Poorichaya Somparn,
  • Daneeya Na Nan,
  • Teerawut Nedumpun,
  • Thanaphum Osathanon,
  • Hiroshi Egusa,
  • Sayamon Srisuwatanasagul,
  • Chenphop Sawangmake

摘要

Background

Small extracellular vesicles (sEVs) derived from mesenchymal stem cells are emerging as promising therapeutic agents in regenerative medicine. This study evaluated the therapeutic potential of sEVs from 3D-cultured canine adipose-derived mesenchymal stem cells in alleviating diabetes-induced systemic dysfunctions, focusing on their revitalizing, metabolic, and immunomodulatory properties.

Results

sEVs were identified as nanosized vesicles around 72 nm with a negative zeta potential (-21.15 mV) and a high particle concentration (1.07 × 109 particles/mL). In vitro, sEVs (104 particles/mL) protected INS-1 β-cells from etoposide (ETO)-induced cytotoxicity, enhancing cell viability, reducing apoptosis, and promoting recovery. Biodistribution analysis showed detectable levels in plasma for up to 24 h post-injection, suggesting sustained circulation and a potentially extended half-life compared to free therapeutic molecules. In streptozotocin (STZ)-induced diabetic mice, sEV treatment significantly improved glycemic control, enhanced glucose metabolism, and restored β-cell function, as reflected by improvements in HOMA-β, HOMA-IR, and QUICKI indices. Additionally, sEVs reduced systemic inflammation, restored immune homeostasis, and improved hematological, renal, and hepatic parameters. Double-dose sEV administration yielded the most pronounced therapeutic benefits, including enhanced glucose clearance and systemic recovery.

Conclusions

sEVs exhibit robust revitalizing, metabolic, and immunomodulatory properties, effectively mitigating diabetes-related dysfunctions in vitro and in vivo. These findings highlight sEVs as a novel regenerative therapy for diabetes and its complications, providing a strong foundation for future clinical translation.