Abstract
Probucol is widely used in clinical treatment as a lipid-reducing and anti-oxidant drug. However, it is unclear whether probucol exerts a renoprotective effect on aging mice. In the present study, we aimed to investigate the effect of probucol on kidneys of D-galactose-induced aging mice and explored the potential mechanisms. The aging mice model was established by subcutaneous injection of D-galactose (100 mg/kg, once daily for 6 weeks). At the end of the 6th week, the mice were administered with probucol or vehicle once daily for 2 weeks. Urine and blood samples as well as kidney tissues were collected for analysis. D-galactose-treated human podocyte cells (HPC) were employed for experiments in vitro. Probucol could improve renal function in D-galactose-induced aging mice, as indicated by reduced blood creatinine and urea nitrogen. Meanwhile, glomerulonephritis progression and podocyte injury were alleviated in probucol-treated mice, as showed by decreased glomerular sclerosis index as well as increased podocyte markers. Besides, probucol ameliorated renal fibrosis and podocyte apoptosis in aging mice. Furthermore, probucol suppressed murine double minute 2 (MDM2) expression, accompanied by the decreased protein level of ERK1/2. Pretreatment with probucol in D-galactose-induced HPC blocked MDM2/ERK1/2 signaling pathway. Thus, probucol ameliorates podocyte injury in D-galactose-induced aging mice by regulating MDM2/ERK1/2 signaling pathway.
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