Previous Exercise Effects in Cisplatin-Induced Renal Lesions in Rats

Abstract

Background/Aims: Physical training has beneficial effects on endothelial function and can influence the regeneration of the endothelial cell. We investigated the effect of physical training on cisplatin (CP)-induced acute kidney injury and assessed the impact of training on endothelial structure and function, and on the inflammatory processes in rats. Methods: We injected male Wistar rats subjected to previous physical training in treadmill running (trained, TR) or not (sedentary, SED) with CP (5 mg/kg) (TR+CP and SED+CP groups, respectively). Five days after the injections, blood and urine samples were collected to evaluate renal function and kidneys were harvested for morphological, immunohistochemical, enzyme-linked immunosorbent assay, and analysis of nitric oxide (NO) levels. Results: Rats treated with CP showed increased levels of plasma creatinine and sodium and potassium fractional excretion. These alterations were associated with increase in tubulointerstitial lesions and macrophage number, reduction of endothelial cells, and increased VEGF, vimentin, and α-smooth muscle actin expression in the outer renal medulla in the SED+CP group. We also found increased levels of renal IL-1β and increased excretion of monocyte chemoattractant protein-1 and transforming growth factor-β compared with controls. These changes were milder in trained rats, associated with increased levels of renal tissue NO, and increased expression of p-eNOS and stromal cell-derived factor-1α (a chemokine involved in kidney repair) in the kidneys of CP-injected trained rats. Conclusions: The protective effect of previous training in CP-treated rats was associated with reduced endothelial cell lesions and increased renal production of NO in trained rats.

Exercise as a therapeutic option for acute kidney injury: mechanisms and considerations for the design of future clinical studies

“…Furthermore, in both instances the effect of exercise was shown in pre-dialysis CKD patients with no studies demonstrating the effects of exercise in the AKI setting. Despite this, the findings are consistent with other work in animal models [23][24][25][26][27][28][29] which have demonstrated an improvement in renal function following exercise in the AKI setting. Although the precise mechanism by which exercise, or increased levels of physical activity may protect against or even promote recovery following AKI in humans remains unclear, one mechanism which may be crucial is the well-reported anti-inflammatory effect of exercise.…”

Renal developmental disturbances and their long-term consequences in female pups from vitamin D-deficient mothers: involved mechanisms

“…15 The number of JG12-positive cells in each cortical interstitial 30-grid field was determined in the renal cortex, and the mean counts were calculated for each section. 16 It has been demonstrated that the semi-quantitative scoring system is not only reproducible among different observers but that data are also highly correlated with those obtained through computerized morphometry by several authors. 17…”

“…To quantify JG12, synaptopodin and cubilin staining, each glomerulus or cortical field (measuring 0.100 mm 2 each) was semi-quantitatively graded, and the mean score per section was calculated. 16 The scores mainly reflected changes in the extent rather than in the intensity of staining and were dependent on the percentage of the glomeruli or grid field, showing positive staining. The scores were determined as follows: 0 = absent or < 5% staining; 1 = 5-25%; 2 = 25-50%; 3 = 50-75% and 4 > 75% staining.…”

Effect of Calcitriol on the Renal Microvasculature Differentiation Disturbances Induced by AT1 Blockade During Nephrogenesis in Rats

“…(36). In vitro and in vivo studies have shown that increased eNOS activity resulted in endothelial cell proliferation and migration, and increased angiogenesis (37,38). Increased NO production in the LOS + Calcitriol group compared to that in the LOS group have resulted in decreased vasoconstriction induced by reduced AT 1 receptor activity in renal tissue from these animals.…”