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EFFECT OF HYPEROSIDE ON KLOTHO PROTEIN IN RATS WITH CHRONIC RENAL FAILURE

LIQIU SUN 1, SHU LI 2, FUBO ZHOU 3, JUN LIANG 4, LEI YAN 5, HONG LI 6*

1Department of Nephrology, The Fourth Hospital of Harbin Medical University, Harbin, 150001, China
2 Department of Medical Function, Mudanjiang Medical University, Mudanjiang, 157011, China
3 Department of Pharmacology, Mudanjiang Medical University, Mudanjiang, 157011, China
4 Stem Cell Institute, Mudanjiang Medical University, Mudanjiang, 157011, China;
5 Department of Histology and Embryology, Mudanjiang Medical University, Mudanjiang, 157011, China
6 Clinical Skills Centre of The First Clinical College, Mudanjiang Medical University, Mudanjiang, Heilongjiang, 157011, China

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This study explored the impact of hyperoside on Klotho protein and its renal protective mechanism in rats with chronic renal failure (CRF). Sixty rats were divided into three groups: normal, model and hyperoside-treated, with 20 rats in each. Renal damage was assessed through haematoxylin and eosin (HE) staining, serum creatinine (SCR), blood urea nitrogen (BUN), total parathyroid hormone (iPTH) levels and the detection of superoxide dismutase (SOD) and malondialdehyde (MDA) in kidney tissues. Additionally, interleukin-1β, interleukin-6 (IL-6) and C-reactive protein (CRP) levels were measured using enzyme-linked immunosorbent assays (ELISA). Results indicated significant increases in SCR, BUN, iPTH, P3+, IL-1β, IL-6, CRP and MDA levels in the model group compared to the normal group, while Ca2+ and SOD levels were decreased (p < 0.05). Hyperoside treatment significantly mitigated these effects, improving both biochemical markers and pathological conditions and notably enhancing Klotho protein expression compared to the model group (p < 0.05). The findings suggest that hyperoside effectively ameliorates CRF, potentially by reducing oxidative stress and microinflammation and by regulating calcium and phosphorus metabolism through Klotho protein expression, thus offering protective effects against renal failure progression.