article · Antioxidants
Cyclosporine A is widely used to suppress the immune system during organ transplantation, but its clinical utility is limited by adverse kidney damage. This study examined whether avocado seed powder could counteract these damaging side effects in rats. Administering cyclosporine caused renal oxidative stress, reduced kidney function, increased DNA damage, and altered related gene expression. Supplementing the animals with a diet containing five percent avocado seed powder for four weeks counteracted these harmful biochemical, molecular, and tissue-level effects. Additionally, the avocado seed powder enhanced the immunosuppressive action of the medication. The findings show that avocado seed powder can protect against cyclosporine-induced kidney toxicity whilst simultaneously supporting its intended immunosuppressive function, suggesting potential utility as a supportive dietary component alongside transplantation therapies.
Organ transplant recipients rely heavily on drugs like cyclosporine to prevent organ rejection, yet the therapy frequently causes severe kidney toxicity. Discovering natural compounds that protect against kidney injury whilst simultaneously strengthening immunosuppression could improve patient outcomes and make long-term transplant management safer and more tolerable.
This work points toward potential applications as an adjunct therapeutic or nutraceutical formulation to be co-administered with immunosuppressive regimens. The prospective users would be pharmaceutical developers or healthcare providers managing organ transplant patients. Because the findings are currently limited to an in vivo animal model, this research remains at an early laboratory stage and requires extensive clinical trials before real-world adoption.
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Cyclosporine A's (CsA) immunosuppressive effect makes it an ideal drug for organ transplantation. However, CsA's uses are restricted due to its side effects. We investigated the effects of avocado seed (AvS) powder on CsA-induced nephrotoxicity and immunosuppression in rats. The injection of CsA (5 mg/kg, subcutaneously, for 10 days) increased serum levels of creatinine, uric acid, and urea, and the renal levels of the malondialdehyde. It decreased creatinine clearance and the renal activity of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and Na<sup>+</sup>/K<sup>+</sup> ATPase. The administration of CsA also significantly downregulated the renal expression of interferon-gamma, tumor necrosis factor-alpha, interleukin 1 beta, monocyte chemotactic protein 1, intercellular adhesion molecule-1, and vascular cell adhesion molecule 1 genes, and increased renal DNA damage. Histopathological examination confirmed the biochemical and molecular alterations that accompanied CsA nephrotoxicity. All CsA-induced deleterious effects, except immunosuppression, were ameliorated by feeding rats on a basal diet supplemented with 5% AvS powder for 4 weeks. Importantly, AvS also maximized CsA's immunosuppressive effect. These findings suggest a potential ameliorative effect of AvS on CsA-induced nephrotoxicity, and AvS enhances CsA's immunosuppressive effect. Therefore, AvS might be used in combination with CsA in transplantation treatment to relieve the CsA-induced nephrotoxicity.
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DOI: 10.3390/antiox10081194
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