Astaxanthin modulates osteopontin and transforming growth factor β1 expression levels in a rat model of nephrolithiasis: a comparison with citrate administration
- To evaluate the effect of astaxanthin on renal angiotensin-I converting enzyme (ACE) levels, osteopontin (OPN) and transforming growth factor β1 (TGF-β1) expressions and the extent of crystal deposition in experimentally induced calcium oxalate kidney stone disease in a male Wistar rat model.
- To compare the efficacy of astaxanthin treatment with a currently used treatment strategy (citrate administration) for kidney stones.
Materials and Methods
- The expression of OPN was assessed by immunohistochemistry. One step reverse transcriptase polymerase chain reaction followed by densitometry was used to assess renal OPN and TGF-β1 levels.
- Renal ACE levels were quantified by an enzyme-linked immunosorbent assay method.
- Crystal deposition in kidney was analysed by scanning electron microscopic (SEM)-energy-dispersive X-ray (EDX).
- The renal ACE levels and the expression of OPN and TGF-β1 were upregulated in the nephrolithiasis-induced rats.
- Astaxanthin treatment reduced renal ACE levels and the expression OPN and TGF-β1.
- SEM-EDX analysis showed that crystal deposition was reduced in the astaxanthin-treated nephrolithiatic group.
- Astaxanthin treatment was more effective than citrate administration in the regulation of renal ACE levels, OPN and TGF-β1 expressions.
- Astaxanthin administration reduced renal calcium oxalate crystal deposition possibly by modulating the renal renin-angiotensin system (RAS), which reduced the expression of OPN and TGF-β1 levels.
- Astaxanthin administration was more effective than citrate treatment in reducing crystal deposition and down-regulating the expression of OPN and TGF-β1.