Preclinical study demonstrates placental mesenchymal stem cells attenuate fibrosis markers in nephrectomized rats, highlighting adiponectin as a monitoring biomarker.
Key Points
To assess the therapeutic potential of amnion-derived mesenchymal stem cells in chronic renal failure and determine if adiponectin serves as a viable biomarker for monitoring progression.
Induced chronic renal failure in male Wistar rats via a two-stage 5/6 nephrectomy procedure over an eight-week observation window.
Administered term placenta amnion-derived mesenchymal stem cells via tail vein injection, evaluating outcomes at 15 and 30 days post-transplantation.
Measured gene and protein levels of Adiponectin, AdipoR1, Fibronectin, and AMPK phosphorylation using RT-PCR and western blot, alongside ELISA assays for urinary albumin and adiponectin.
Subtotal nephrectomy induced significant elevations in the mRNA and protein expressions of Adiponectin, AdipoR1, Fibronectin, and phosphorylated AMPK compared to controls.
Transplantation of placental mesenchymal stem cells reversed these pathologic elevations, causing a marked decline in Adiponectin, AdipoR1, Fibronectin, and AMPK phosphorylation across follow-up intervals.