article · Membranes
Research examining the impact of extracellular vesicles on diabetic nephropathy evaluated the therapeutic effects of camel milk and its exosomes in a streptozotocin-induced diabetic rat model. Treatment using camel milk, its exosomes, or both interventions together counteracted diabetic kidney damage across several physiological measures. Treated animals showed marked reductions in kidney function markers such as urea, creatinine, urinary proteins, and retinol-binding protein. The interventions also restored redox balance by lowering lipid peroxidation and raising the activity of antioxidant enzymes, including catalase, superoxide dismutase, and glutathione peroxidase. Furthermore, treatment downregulated the expression of renal injury genes, including kidney injury molecule-1 and transforming growth factor-beta 1, while reducing histological damage scores. The combined administration of camel milk and its exosomes demonstrated the strongest ameliorative effect.
Diabetic nephropathy is a serious complication of diabetes that often leads to chronic kidney failure. Understanding how biological components like camel milk and milk-derived extracellular vesicles protect renal tissues offers valuable insight. The findings show that these treatments can target both oxidative stress and gene pathways associated with kidney damage, supporting future exploration into managing diabetic complications.
This research could eventually inform the development of biological therapies, nutraceuticals, or exosome-based drug delivery systems for kidney protection in diabetic patients. Likely users include biopharmaceutical firms and biotechnology developers exploring renal therapeutics. As the findings are based entirely on an early-stage laboratory study in a streptozotocin-induced rat model, the approach remains far from real-world clinical application and requires substantial translational testing.
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Contradictory results were obtained regarding the effects of extracellular vesicles such as exosomes (EXOs) on diabetes and diabetic nephropathy (DN). Some studies showed that EXOs, including milk EXOs, were involved in the pathogenesis of DN, whereas other studies revealed ameliorative effects. Compared to other animals, camel milk had unique components that lower blood glucose levels. However, little is known regarding the effect of camel milk and its EXOs on DN. Thus, the present study was conducted to evaluate this effect on a rat model of DN induced by streptozotocin. Treatment with camel milk and/or its EXOs ameliorated DN as evidenced by (1) reduced levels of kidney function parameters (urea, creatinine, retinol-binding protein (RBP), and urinary proteins), (2) restored redox balance (decreased lipid peroxide malondialdehyde (MDA) and increased the activity of antioxidants enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)), (3) downregulated expression of DN-related genes (transforming growth factor-beta 1 (<i>TGFβ1</i>), intercellular adhesion molecules 1 (<i>ICAM1</i>), and transformation specific 1 (<i>ETS1</i>), integrin subunit beta 2 (<i>ITGβ2</i>), tissue inhibitors of matrix metalloproteinase 2 (<i>TIMP2</i>), and kidney injury molecule-1 (<i>KIM1</i>)), and (4) decreased renal damage histological score. These results concluded that the treatment with camel milk and/or its EXOs could ameliorate DN with a better effect for the combined therapy.
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DOI: 10.3390/membranes12111060
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