Activation of peroxisome proliferator-activated receptor delta inhibits @entity3839 -induced @entity2316 through anti-inflammatory mechanisms in XXXX .

@entity3229 @entity6 @entity1750 @entity2316 @entity19 @entity3839 @entity1189 @entity26221 @entity413
OBJECTIVE: Activation of the nuclear hormone receptor peroxisome proliferator-activated receptor ( @entity3229 )-   has been shown to improve insulin resistance, adiposity, and plasma HDL levels. Several studies have reported that activation of @entity3229   is atheroprotective; however, the role of @entity3229   in renal function remains unclear. Here, we report the renoprotective effects of @entity3229   activation in a model of @entity3839 -induced @entity2316 . RESEARCH DESIGN AND METHODS: Eight-week-old male C57BL/6 @entity19 were divided into three groups: 1) nondiabetic control @entity19 , 2) @entity6 @entity19 , and 3) @entity6 @entity19 treated with the @entity3229   agonist @entity26221 (1 mg/kg/day). @entity26221 was administered by gavage for 8 weeks after inducing @entity6 . RESULTS: @entity26221 decreased urinary albumin excretion without altering blood @entity413 levels. Macrophage infiltration, mesangial matrix accumulation, and type IV collagen deposition were substantially attenuated by @entity26221 . The gene expression of inflammatory mediators in the kidney cortex, such as @entity1750 ( @entity1750 ) and @entity1189 ( @entity1189 ), was also suppressed. In vitro studies demonstrated that @entity3229   activation increased the expression of anti-inflammatory corepressor B-cell lymphoma-6, which subsequently suppressed @entity1750 and @entity1189 expression. CONCLUSIONS: These findings uncover a previously unrecognized mechanism for the renoprotective effects of @entity3229   agonists and support the concept that @entity3229   agonists may offer a novel therapeutic approach for the treatment of @entity2316 .
