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Updated: Jul 28, 2025
Prospective, Randomized, and Controlled Study of a Human Umbilical Cord Mesenchymal Stem Cell Injection for Treating Diabetic Foot Ulcers
Published on: March 3, 2023
Human umbilical cord-derived mesenchymal stem cells alleviate oxidative stress-induced islet impairment via the
Peng Liu1, Baige Cao2, Yang Zhou3
1Shanghai Diabetes Institute, Department of Endocrinology and Metabolism, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China.
Abstract:
Hyperglycaemia-induced oxidative stress may disrupt insulin secretion and β-cell survival in diabetes mellitus by overproducing reactive oxygen species. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) exhibit antioxidant properties. However, the mechanisms by which hUC-MSCs protect β-cells from high glucose-induced oxidative stress remain underexplored. In this study, we showed that intravenously injected hUC-MSCs engrafted into the injured pancreas and promoted pancreatic β-cell function in a mouse model of type 1 diabetes mellitus. The in vitro study revealed that hUC-MSCs attenuated high glucose-induced oxidative stress and prevented β-cell impairment via the Nrf2/HO-1 signalling pathway. Nrf2 knockdown partially blocked the anti-oxidative effect of hUC-MSCs, resulting in β-cell decompensation in a high-glucose environment. Overall, these findings provide novel insights into how hUC-MSCs protect β-cells from high glucose-induced oxidative stress.
Insights
Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) protect pancreatic beta cells from high glucose damage. These stem cells activate the Nrf2/HO-1 pathway, crucial for antioxidant defense in diabetes mellitus.
Area of Science:
- Stem cell biology
- Endocrinology
- Oxidative stress research
Background:
- Hyperglycemia in diabetes mellitus causes oxidative stress, impairing insulin secretion and beta-cell survival.
- Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) possess known antioxidant properties.
- The precise mechanisms of hUC-MSC protection against high glucose-induced beta-cell damage are not fully understood.
Purpose of the Study:
- To investigate the protective effects of hUC-MSCs on pancreatic beta cells under high glucose conditions.
- To elucidate the underlying molecular mechanisms, particularly the role of the Nrf2/HO-1 signaling pathway.
Main Methods:
- Utilized a mouse model of type 1 diabetes mellitus.
- Administered hUC-MSCs intravenously to assess pancreatic engraftment and beta-cell function.
- Conducted in vitro experiments to examine hUC-MSC effects on beta-cells exposed to high glucose.
- Investigated the Nrf2/HO-1 pathway, including Nrf2 knockdown studies.
Main Results:
- Intravenously injected hUC-MSCs engrafted into the injured pancreas and improved beta-cell function in diabetic mice.
- In vitro, hUC-MSCs mitigated high glucose-induced oxidative stress and prevented beta-cell impairment.
- The Nrf2/HO-1 signaling pathway was identified as the key mediator of hUC-MSC antioxidant effects.
- Nrf2 knockdown partially abrogated the protective effects of hUC-MSCs, leading to beta-cell decompensation.
Conclusions:
- hUC-MSCs offer a promising therapeutic strategy for protecting pancreatic beta cells against hyperglycemia-induced oxidative stress.
- The Nrf2/HO-1 pathway is essential for mediating the antioxidant and cytoprotective effects of hUC-MSCs in diabetes.
- These findings provide critical insights into stem cell-based therapies for diabetes mellitus.
