ISSN:
1437-7799
Keywords:
Key words IgA nephropathy
;
Rats
;
Oxidative stress
;
Malondialdehyde
;
TGFβ1 mRNA
;
α-Tocopherol
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Background. We have previously shown that α-tocopherol prevents oxidative stress in experimental IgA nephropathy (IgAN) when administered before or concurrent with the induction of IgAN. We now seek to determine whether α-tocopherol can ameliorate the disease after IgAN is established. Methods. Using the classic IgAN model, 25 male Lewis rats were sorted into five groups of five animals each: 4-week control, 4-week bovine gamma globulin (BGG) treatment, 6-week control, 6-week BGG treatment, and 6-week BGG treatment with α-tocopherol administration started after 4 weeks. Serum α-tocopherol concentrations, kidney and plasma malondialdehyde concentrations, and kidney transforming growth factor beta-1 (TGFβ1) mRNA were analyzed. Results.α-Tocopherol modulated IgAN after the disease was established in the 4-week BGG model, as indicated by the reduction in tissue oxidative stress, dampening of fibrogenic cytokine (TGFβ1), and abatement of proteinuria in α-tocopherol-treated animals compared with untreated rats. Conclusions. These results substantiate the anti-oxidant role of α-tocopherol in diminishing the indices associated with progression of experimental IgAN. The ability of α-tocopherol to reduce the progression of injury after establishment of the disease reflects the clinical situation, and thus holds promise for human therapy.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s101570070020
Permalink
