Astaxanthin modulates osteopontin and transforming growth factor β1 expression levels in a rat model of nephrolithiasis: a comparison with citrate administration.
OBJECTIVE
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.


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).


RESULTS
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.


CONCLUSIONS
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.
School of Biosciences, Mahatma Gandhi University, Kottayam, Kerala, India.
Manju
M
Alex
M V
MV
Sauganth Paul
M
M
Abhilash
Varghese V
VV
Mathews
T V
TV
Anilkumar
R Harikumaran
RH
Nair
D000818:Animals; D002614:Chelating Agents / Q000494:pharmacology; D019343:Citric Acid / Q000008:administration & dosage / Q000494:pharmacology*; D004195:Disease Models, Animal; D015536:Down-Regulation; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology*; D008297:Male; D053040:Nephrolithiasis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053495:Osteopontin / Q000187:drug effects* / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000187:drug effects* / Q000378:metabolism; D024341:Xanthophylls / Q000494:pharmacology
D002614:Chelating Agents; D053773:Transforming Growth Factor beta1; D024341:Xanthophylls; D053495:Osteopontin; D019343:Citric Acid; C005948:astaxanthine; D007703:Peptidyl-Dipeptidase A
angiotensin converting enzyme; astaxanthin; nephrolithiasis; osteopontin