Kidney injury markers, an oxidative stress marker, and inflammation markers were measured in 36-week-old rats. KIM1 is located in the renal proximal tubule epithelial cells, and urinary KIM1 is a specific biomarker for tubular injury. Thirty-six-week-old male human apoB Tg. SHR-cp/cp rats showed higher urinary KIM1 levels when fed the western diet than an established diabetic nephropathy model, non-Tg. SHR-cp/cp rats (Fig. 2A
Fig. 2. Kidney injury, oxidative, and inflammation marker levels in 36-week-old of human apoB Tg. SHR-cp/cp (n=9), non-Tg. SHR-cp/cp (n=8), human apoB Tg. SHR-+/+ (n=7), and non-Tg. SHR-+/+ rats (n=7). (A) Urinary KIM1 excretion, (B) Spp1 mRNA expression in the kidney cortex, (C) plasma thiobarbituric acid reactive substances (TBARS), and (D) plasma C-reactive protein (CRP) levels. The asterisks indicate a significant difference at *P<0.05 or **P<0.01 in comparison of human apoB Tg. SHR-cp/cp rats with their littermates.). SPP1 is a pleiotropic cytokine that is ubiquitously expressed and upregulated during inflammation. Thirty-six-week-old male human apoB Tg. SHR-cp/cp rats also showed increased Spp1 mRNA expression levels in the renal cortex; compared with non-Tg. SHR-cp/cp rats (Fig. 2B). The plasma levels of TBARS, an oxidative stress marker and an index for lipid peroxidation are shown in Fig. 2C. Thirty-six-week-old male human apoB Tg. SHR-cp/cp rats showed more than a three-fold increase in TBARS levels than their littermates, human apoB Tg. SHR-+/+, non-Tg. SHR-cp/cp, and non-Tg. SHR-+/+ rats (Fig. 2C). The plasma levels of CRP, a sensitive marker for inflammation, are shown in Fig. 2D. Thirty-six-week-old male human apoB Tg. SHR-cp/cp rats showed significantly increased plasma hsCRP levels than those of their littermates, human apoB Tg. SHR-+/+, non-Tg. SHR-cp/cp, and non-Tg. SHR-+/+ rats (Fig. 2D).