Effects of inflammatory response on renal function and TGF-β1 pathway of rats with aging-related kidney damage by upregulating the expression of CD36.

Abstract

The aim of this study was to explore the effects of inflammatory response on renal function and TGF-β1 pathway of rats with aging-related kidney damage by upregulating the CD36 expression. A total of 70 pathogen free (PF) Sprague-Dawley (SD) male rats were enrolled. The rats injected with normal saline and D-galactose were assigned to a control group and a model group, respectively. Those injected with both D-galactose and different concentrations of casein were assigned to casein A, B, and C groups accordingly, and 16 rats injected with D-galactose and with CD36 gene knocked out were assigned to a treatment group. The following methods were employed to determine the following factors of the rats: ELISA for serum inflammatory factors, Western blot for CD36 in kidney tissues, Real Time-PCR for TGF-β1, and Smad (2, 3, and 7) mRNA, radioimmunoassay for hyaluronic acid (HA) and laminin (LN), and colorimetry for the expression quantity of plasma superoxide dismutase (SOD) and malondialdehyde (MDA). An automatic biochemical analyzer was used to determine blood, urine, and renal function indexes. After successful modeling, the model group showed significantly higher inflammatory indexes than the control group. The relative expression of CD36 in the model group was significantly higher than that in the control group and treatment group, and significantly lower than that in the casein groups. Both inflammatory indexes and relative expression of CD36 increased with the increase of casein concentration in the casein groups. Groups with severer inflammatory response showed higher renal function indexes, and higher expression of TGF-β1, Smad2, Smad3, HA, LN, and MDA, and those with decreased CD36 level showed lower renal function index levels. The Smad7 expression and SOD were contrary. Inflammatory stress can promote the CD36 expression in renal tissues of aging rats and oxidative stress and affect TGF-β1/Smad pathway, thus aggravating renal fibrosis and renal damage in rats.