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Stem Cells Derived From Human Deciduous Exfoliated Teeth Ameliorate Adriamycin-induced Nephropathy In Rats By
Yuyang Dai1, Borui Tang1,2, Xiuli Zhao1
1National Institute for Drug Clinical Trial, Beijing Tongren Hospital, Capital Medical University, No.1 Dongjiaominxiang Road, Beijing, 100730, China.
Insights
Stem cells from human exfoliated deciduous teeth (SHEDs) show therapeutic potential for kidney injury in a rat model. SHED transplantation reduced proteinuria, inflammation, and immune imbalance, suggesting a novel treatment for nephrotic syndrome.
Area of Science:
- Nephrology
- Stem Cell Biology
- Immunology
Background:
- Idiopathic Nephrotic Syndrome (INS) is a common childhood kidney disease characterized by hypoproteinemia, proteinuria, hyperlipidemia, and edema.
- Mesenchymal Stem Cells (MSCs) possess tissue repair, anti-fibrotic, and immunomodulatory properties, but their role in INS is underexplored.
Purpose of the Study:
- To investigate the therapeutic efficacy of stem cells from human exfoliated deciduous teeth (SHEDs) in an adriamycin-induced nephropathy (AN) rat model.
- To explore the potential of SHEDs in treating kidney injury and associated immune dysregulation.
Main Methods:
- Adriamycin-induced nephropathy (AN) model in Sprague-Dawley rats.
- SHED transplantation via tail vein (single and multidose regimens).
- Assessment of kidney function, histological damage, fibrosis, immune cell infiltration (T lymphocytes), podocyte integrity, inflammatory markers (IL-6, TNF-α, IL-1β), and Th17/Treg cell balance.
Main Results:
- SHEDs demonstrated targeted migration to damaged kidney tissues.
- SHED transplantation significantly reduced proteinuria, reversed biochemical abnormalities, and inhibited glomerular/tubular damage and fibrosis.
- SHEDs protected podocytes, reduced inflammation, and corrected immune imbalances by modulating Th17/Treg cell populations.
Conclusions:
- SHED transplantation partially suppressed inflammation and alleviated kidney injury in the AN rat model.
- Immune regulation is a key mechanism underlying the therapeutic effects of SHEDs in nephrotic syndrome.
Background:
Idiopathic Nephrotic Syndrome (INS) is a common kidney disease in children, and the main clinical manifestations are hypoproteinaemia, proteinuria, hyperlipidaemia, and oedema. Mesenchymal Stem Cells (MSCs) are involved in tissue repair, protection against fibrosis, and immune modulation but have rarely been studied in INS.
Objective:
This study aimed to explore the therapeutic potential of stem cells derived from human exfoliated deciduous teeth (SHEDs) in INS using an adriamycin-induced nephropathy (AN) rat model.
Methods:
AN was induced in Sprague‒Dawley rats, and SHEDs were transplanted via the tail vein in single (SHED-s) and multidose (SHED-m) regimens. Cell migration assays were used to track the SHED distribution. Weight, urine protein, and serum biochemical assays were also performed. HE and Masson staining were used to observe glomerular and tubular damage, as well as the degree of fibrosis. Immunohistochemistry was used to label T lymphocytes and podocytes, and structural changes in podocytes were observed by electron microscopy. ELISA was used to measure the levels of inflammatory factors. Flow cytometry was used to analyse the balance of Th17 cells and Tregs. The mRNA expression of Th17- and Treg-associated cytokines and specific transcription factors was examined by RT‒PCR.
Results:
SHEDs directly migrated to damaged tissues, suggesting a targeted therapeutic effect. SHED transplantation significantly reduced proteinuria and reversed biochemical abnormalities in rats with AN. Both single and multidose SHED treatments could inhibit glomerular and tubular damage and delay the progression of fibrosis caused by adriamycin. SHEDs exerted a protective effect on podocytes. Additionally, this treatment inhibited inflammatory responses and corrected immune imbalances, as evidenced by decreased T lymphocyte infiltration, reduced serum levels of IL-6, TNF-a, and IL-1β, and modulation of the Th17/Treg balance.
Conclusion:
In the AN rat model, SHED partly suppressed the development of inflammation and alleviated kidney injury, and immune regulation may be the underlying mechanism.
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