The effect of exercise on reelin level in the hippocampus of diabetic rats.

AIM: Diabetes is one of the most common diseases which can attenuate brain function by destroying hippocampus neurons, while reelin is a largely secreted extracellular matrix glycoprotein in the hippocampus causing synaptic plasticity, promoting postsynaptic structures and maturing neurons. The aim of this study was to assess the effect of exercise, as an external factor for neurogenesis in the brain, on reelin levels and memory improvement in diabetic rats. METHOD: Thirty rats were randomly allocated into three groups; healthy sedentary, diabetic sedentary and diabetic exercise-trained. The experimental group was treadmill-exercised at speed 22 m/min for 1 hour, 5 days per week. Finally, spatial memory of rats was tested and reelin levels were measured. RESULTS: The results showed that short-term exercise improved spatial memory in diabetic rats but had no effect on reelin levels in the hippocampus of diabetic rats. CONCLUSION: Diabetes reduced the spatial memory without altering the reelin levels while exercise improved spatial memory without altering the reelin levels (Fig. 4, Ref. 33).

EFFECTS OF EXERCISE ON MIR-29 AND IGF-1 EXPRESSION AND LIPID PROFILE IN THE HEART OF OVARIECTOMIZED RAT.

INTRODUCTION: Menopause increases the risk of cardiovascular disease in women. The aims of the present study were to evaluate the effects of swimming training on cardiac histology and expression of miR-29 and IGF-1 in the ovariectomized rats. MATERIALS AND METHODS: Thirty female Wistar rats were divided into sham and ovariectomized groups: sedentary control (OVX) and trained with 8 weeks exercise (OVX.E). On 57th day, blood was collected and used for lipid profile measurement. In addition, heart tissue was analyzed by reverse transcription-polymerase chain reaction for IGF-1 mRNA and miR-29, and studied for histopathological changes. RESULTS: Ovariectomy significantly decreased miR-29 and IGF-1 expression in the heart compared to sham animals group (p<0.05). Exercise training increased miR-29 and IGF-1 expression in the trained rats and improved histology and lipid profile compared with OVX group (p<0.05). CONCLUSION: Estrogen deficiency could lead to cardiac fibrosis through deregulation miR-29 and IGF-1 expression. The findings of the current study suggests a protective effect of exercise on heart against fibrotic changes in ovariectomized rats and support a potential preventive value of exercise in improving cardiac function after menopause.

Effects of noradrenaline and KCl on peripheral vessels in doxorubicin induced model of heart failure.

The purpose of the work presented here was to investigate the responses mediated by alpha-adrenoceptors and also contractility of vascular smooth muscle in large peripheral vessels following doxorubicin (DXR)-induced heart failure. Cardiac failure was induced by DXR injection. Thirty saline-treated (normal group) and 30 DXR-treated rabbits (1 mg/kg administered intravenously twice weekly for 8 weeks) were studied. Chronic heart failure was confirmed by echocardiography and later also by histopathology. The DXR-treated hearts were subdivided by ejection fraction >40 or <40 into non-failing (control) and failing (test) groups. Animals were sacrificed by overdose with pentobarbitone sodium (i.v. injection). Arteries and veins were carefully removed with as little connective tissue as possible and placed in cold physiological salt solution. The arterial and venous rings were mounted in 10 ml isolated organ baths, maintained at 37 degrees C and gassed with 95% O(2) plus 5% CO(2). The rings were then placed under different resting tensions. After initial application of tension tissues were left to equilibrate for a 60-min period. Then all preparations were contracted with KCl (Krebs solution, Na free and high KCl, 125 mM) and allowed to contract for 5-10 min. Following complete washout with normal Krebs, an additional 30 min equilibration period was allowed. Then cumulative concentration-response curves to noradrenaline (NA) obtained by increasing the concentration of the agonist in half-log increments. In contraction responses to NA the renal artery and aorta were the most sensitive preparations (pD(2) values: 5.75 and 5.36, respectively). Compared with control, in DXR-treated rabbits, maximum response (E(max)) of NA was not modified in the aorta; renal and saphenous arteries, renal and saphenous veins, whereas it was significantly lower in the vena cava. Compared with control rabbits, in DXR-treated rabbits the pD(2) of NA was significantly increased in the thoracic aorta whereas there was no significant difference between groups in the other studied vessels. Contraction to KCl showed no significant difference between two groups. These results suggest that the sympathetic regulation of vascular contraction is impaired by DXR-induced heart failure through reduction in the alpha-adrenoceptors.