Validation experiment designed to validate causal mechanisms targeting ACAT1 in folic acid-induced nephropathy mice. Primary outcome: reduction in renal fibrosis and mitochondrial injury
Mouse model of chronic kidney disease was established using folic acid administration to induce nephropathy. Mice were treated with hyperoside to evaluate its renoprotective effects against kidney fibrosis. The study assessed mitochondrial function, lipid metabolism, and fibrotic progression through histological evaluation, biochemical analyses, and electron microscopy. Multi-omics approaches including transcriptomics and metabolomics were employed to characterize metabolic pathway modulation by hyperoside treatment.
folic acid administration to induce nephropathy, hyperoside treatment, histological evaluation, biochemical analyses, electron microscopy, transcriptomic and metabolomic analyses
hyperoside would reduce renal fibrosis and improve mitochondrial function
significant reduction in fibrotic markers and improved mitochondrial morphology and function
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