Study of Histopathological and Molecular Changes of Rat Kidney under Simulated Weightlessness and Resistance Training Protective Effect

Abstract

To explore the effects of long-term weightlessness on the renal tissue, we used the two months tail suspension model to simulate microgravity and investigated the simulated microgravity on the renal morphological damages and related molecular mechanisms. The microscopic examination of tissue structure and ultrastructure was carried out for histopathological changes of renal tissue morphology. The immunohistochemistry, real-time PCR and Western blot were performed to explore the molecular mechanisms associated the observations. Hematoxylin and eosin (HE) staining showed severe pathological kidney lesions including glomerular atrophy, degeneration and necrosis of renal tubular epithelial cells in two months tail-suspended rats. Ultrastructural studies of the renal tubular epithelial cells demonstrated that basal laminas of renal tubules were rough and incrassate with mitochondria swelling and vacuolation. Cell apoptosis in kidney monitored by the expression of Bax/Bcl-2 and caspase-3 accompanied these pathological damages caused by long-term microgravity. Analysis of the HSP70 protein expression illustrated that overexpression of HSP70 might play a crucial role in inducing those pathological damages. Glucose regulated protein 78 (GRP78), one of the endoplasmic reticulum (ER) chaperones, was up-regulated significantly in the kidney of tail suspension rat, which implied that ER-stress was associated with apoptosis. Furthermore, CHOP and caspase-12 pathways were activated in ER-stress induced apoptosis. Resistance training not only reduced kidney cell apoptosis and expression of HSP70 protein, it also can attenuate the kidney impairment imposed by weightlessness. The appropriate optimization might be needed for the long term application for space exploration.

Simulated microgravity‐induced mitochondrial dysfunction in rat cerebral arteries

“…Mitochondrial dysfunction has been reported to contribute to vascular oxidative stress and vasoreactivity alterations (34–36). Although further evidence is needed, structural changes in mitochondria have been found in simulated microgravity, and mitochondrial disassembly in vascular endothelial cells (24), mitochondria swelling and vacuolation in the kidney (37), and higher mitochondrial volume densities and mitochondria‐to‐myofibril ratios in myocardium (38) have been observed. However, evidence of mitochondrial dysfunction remains scare, and whether dysfunctional mitochondria contribute to vascular oxidative stress injury is unknown.…”

Protective Effect of Aerobic Exercise Against L-Name-Induced Kidney Damage in Rats

“…Hägg et al (4) have also demonstrated that exercise downregulates overexpression of aortic HSP70 in spontaneously hypertensive rats (4), and Ding et al (31) found a reduction in renal expression of HSP70 and in cell apoptosis in kidney-impaired rats. De Moraes et al (28) proposed that increases in cardiac output during exercise, associated with renal vasoconstriction and upregulation of endothelial NOS, could enhance blood fl ow velocity and shear stress in kidney circulation.…”

Antimicrobial activity and safety evaluation of peptides isolated from the hemoglobin of chickens

“…Both transmission electron microscopy (TEM) and scanning electron microscopy (SEM) were conducted as previously described [32–34]. Briefly, Escherichia coli ATCC 25922 and Staphylococcus aureus ATCC29213 were cultured overnight, 10 7  CFU ml −1 bacteria were incubated with 1 × MIC of CHAP or diluents of the same volume at 37 °C for 30 min.…”