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Abstract
The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate
in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated
diabetic rats. Diabetic rats were divided into two groups: aminoguanidine treated
group (25 mg/kg body wt, daily i.p. injection; DM-AG group) and untreated group (DM
group). Non-diabetic age-matched rats were also divided into two groups with the same
manner and used as controls. After twelve weeks of treatment, glomerular basement
membranes (GBM) were isolated from rats of each experimental group. When thioglycollate-elicited
peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials,
GBM from DM group induced significantly greater levels of TNF and IL-1 production
than did GBM from other three groups with at doses of 2.5 to 10 mg. The TNF and IL-1
production by stimulation of GBM from the DM-AG group were similar to those from each
control group. Aminoguanidine treatment significantly decreased the accumulation of
advanced glycation end-products (AGEs) in GBM of diabetic rats. These findings suggest
that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. AGE-induced
cytokines may be implicated in the development of diabetic nephropathy.