Ang II induce kidney damage by recruiting inflammatory cells and up regulates PPAR gamma and Renin 1 gene: effect of β carotene on chronic renal damage

Antioxidants are widely used for prevention of diseases associated with oxidative stress and ischemic disorder. We investigated the hypothesis of antioxidants (α-tocopherol and β-carotene) can suppress the renal disorder in apo E-/-mice. Renal damage induced by chronic infusion of Angiotensin II (Ang II) into 4 month old male apo E-/-mice. After that the mice were treated with diet enriched α tocopherol and β carotene (800 mg/kg) for 150 days. Ang II treated kidney showed polycystic appearance with accumulation of clear fluid and constriction of renal artery and renal vein was noticed. Vacuolar/cystic degeneration as well as inflammatory reactions was noticed in the tubules/glomerulus of Ang II treated mice. β carotene treated mice showed enormous numbers of regenerated tubules in the kidney and over expression of ICAM proteins in the regenerated tubules. CD 45.2, MAC 3 proteins were over expressed in the inflammatory cells infiltrated into the tubular region of Ang II treated kidney. Gene expression studies revealed up regulation of Renin 1 (Ren 1) and PPARγ genes in the kidney of Ang II treated animals, but the β carotene treatment controlled the expression of these genes in the regenerated kidneys. β carotene may have protective effective on chronic renal disorder. It may repress the inflammatory genes (Ren 1, PPARγ) to achieve the protective effect on Ang II induced renal damage.