Abstract
The purpose of this study was to evaluate the effects of exercise training on renal fibrosis in hypertensive rats. Masson’s trichrome staining and Western blotting were performed on the excised renal cortex from sixteen male spontaneously hypertensive rats (SHR), which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on an exercise treadmill for 60 min/day, 5 sessions/week, for 12 weeks), and from eight male Wistar-Kyoto rats which served as a sedentary normotensive group (WKY). The systolic blood pressure (SBP) and renal fibrosis in hypertensive rats improved after exercise training. The inflammatory-related protein levels of interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2), as well as the fibrotic-related protein levels of transforming growth factor-beta (TGF-β), phospho-Smad2/3 (p-Smad2/3), connective tissue growth factor (CTGF), matrix metalloproteinase-9 (MMP-9), and matrix metalloproteinase-2 (MMP-2) were decreased in the SHR-EX group when compared with the SHR group. Exercise training suppressed the hypertension-induced renal cortical inflammatory and fibrotic pathways in hypertensive rat models. These findings might indicate a new therapeutic effect for exercise training to prevent renal fibrosis in hypertensive nephropathy.
Highlights
Hypertensive nephropathy is the second leading cause of end-stage renal disease, and its prevalence continues to rise worldwide [1,2]
There were no significant differences in whole kidney weight (WKW) and whole kidney weight/tibia length (WKW/TL) among the three groups (Table 1)
After 12 weeks of exercise training, the final systolic blood pressure (SBP) significantly decreased in the spontaneously hypertensive rats (SHR)-EX group when compared with the SHR group (Table 1)
Summary
Hypertensive nephropathy is the second leading cause of end-stage renal disease, and its prevalence continues to rise worldwide [1,2]. Another study showed that renal cortical expression of cyclooxygenase-2 (COX-2) was upregulated in a salt -induced hypertension diet that may play a role in the pathogenesis of hypertensive renal injury [9]. This indicates that the activation of leukocytes and certain cytokines propagate a state of chronic inflammation in hypertensive nephropathy patients, which likely contributes to the progression of chronic kidney disease and end-stage renal disease [10,11]. Previous studies showed that transforming growth factor (TGF)-β1 expression favors excessive accumulation of extracellular matrix proteins that characterize glomerular and tubulointerstitial cells in hypertensive rats with moderate renal damage [14]. We hypothesized that exercise training might suppress renal inflammatory conditions and the TGF-β/CTGF-mediated renal fibrotic pathways in hypertension
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