Imatinib ameliorates renal disease and survival in murine lupus autoimmune disease.

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Another use for Imatinib in the works.

Zavie

" " Platelet-derived growth factor (PDGF) has been proved to play an

important role in progressive glomerular disease of systemic lupus. The

present study investigated the tyrosine kinase inhibitor of PDGF

receptor, imatinib, as a novel therapeutic approach for the cure of

lupus nephritis in New Zealand Black/White (NZB/W)F1 hybrid mice with

established disease " "

" " findings of amelioration of animal survival and renal manifestations

in NZB/W lupus mice with established disease by imatinib suggests the

possibility to explore whether imatinib may function as steroid-sparing

drug in human lupus nephritis. " "

2006 May 10;

Imatinib ameliorates renal disease and survival in murine lupus

autoimmune disease.

Zoja C, Corna D, Rottoli D, Zanchi C, Abbate M, Remuzzi G.

1 Negri Institute for Pharmacological Research, Bergamo, Italy.

Platelet-derived growth factor (PDGF) has been proved to play an

important role in progressive glomerular disease of systemic lupus. The

present study investigated the tyrosine kinase inhibitor of PDGF

receptor, imatinib, as a novel therapeutic approach for the cure of

lupus nephritis in New Zealand Black/White (NZB/W)F1 hybrid mice with

established disease. Two groups of NZB/W mice (N=30 each group),

starting at 5 months of age, were given by gavage vehicle or imatinib

(50 mg/kg b.i.d). Fifteen mice for each group were used for the survival

study. The remaining were killed at 8 months. Imatinib significantly

(P=0.0022) ameliorated animal survival with respect to vehicle. The drug

significantly delayed the onset of proteinuria (% proteinuric mice, 7

and 8 months: 33 and 47 vs vehicle, 80 and 87, P<0.05) and limited the

impairment of renal function. Imatinib protected the kidney against

glomerular hypercellularity and deposits, tubulointerstitial damage, and

accumulation of F4/80-positive mononuclear cells and alpha-smooth

actin-positive myofibroblasts. The abnormal transforming growth

factor-beta mRNA expression in kidneys of lupus mice was reduced by

imatinib. In conclusion, findings of amelioration of animal survival and

renal manifestations in NZB/W lupus mice with established disease by

imatinib suggests the possibility to explore whether imatinib may

function as steroid-sparing drug in human lupus nephritis.

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