New Findings r What is the central question of this study?Could the activation of oxytocin or oestrogen receptors be protective against myocardial injury after ovariectomy? If so, would exercising have an additional ameliorating effect? r What is the main finding and its importance?The results revealed that when accompanied by exercise, both oestrogen receptor agonists and oxytocin improved cardiac dysfunction, inhibited the generation of pro-inflammatory cytokines and reduced myocardial injury in ovariectomized female rats, suggesting a new approach for protecting postmenopausal women against ischaemia-induced myocardial injury.To investigate the putative protective effects of oxytocin or oestrogen receptor agonists against myocardial injury of ovariectomized sedentary or exercised rats, female Sprague-Dawley rats assigned to sham-operated control and ovariectomized (OVX) groups were kept sedentary or undertook swimming exercise for 4 weeks and were treated with saline, an oestrogen receptor (ER) β (DPN) or ERα agonist (PPT) or oxytocin. Ovariectomy increased weight gain and anxiety in sedentary rats, whereas exercise prevented weight gain. When accompanied by exercise, both ER agonists and oxytocin inhibited weight gain and anxiety; oxytocin, in the absence or presence of exercise, increased the left ventricular diastolic dimensions and ejection fraction, whereas ER agonists also increased left ventricular diameter when given to exercised rats. Upon the induction of myocardial ischaemia-reperfusion in the OVX rats, plasma creatine kinase-(muscle-brain) was depressed by PPT and oxytocin, whereas DPN, PPT and OT reduced plasminogen activator inhibitor-1 concentrations. The increased tumour necrosis factor-α concentration in OVX rats was also suppressed by exercise or DPN, PPT or oxytocin treatments, whereas the interleukin-6 concentration was diminished by all the treatments when given in conjunction with exercise. Disorganization of cardiac muscle fibres was reduced in all exercised rats. Oestrogen receptor agonists, as well as oxytocin, in conjunction with exercise may be effective new therapeutics to protect against myocardial ischaemia in postmenopausal women.

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Objective: Sepsis leads to conditions such as inflammatory and anti-inflammatory process, circulatory abnormalities, cellular and humoral reactions. Endotoxin-induced oxidative stress causes injury in the liver. The aim of this study was to evaluate the effects of a radical scavenger Tempol in lipopolysaccharide (LPS)-induced liver injury in rats. Materials and Methods: Male Wistar rats were divided into four groups: Control, LPS (15 mg/kg), LPS + Tempol group (100 mg/kg Tempol, three hours after LPS administration) and Tempol (100 mg/kg). Blood glucose and body temperature were measured during the experiment. Superoxide dismutase (SOD), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and C-reactive protein (CRP) levels were measured in plasma or liver tissue. Furthermore, histopathological changes and myeloperoxidase-stained leukocytes infiltration were assessed in liver tissue. Results: LPS caused tissue damage and leukocytes infiltration, increased AST, ALT and CRP levels, and decreased body temperature, blood glucose and SOD levels. Tempol reduced AST and ALT levels and increased SOD levels. Tempol did not prevent tissue damage, leukocytes infiltration and increment of CRP levels. There were no changes in body temperature and blood glucose levels. Conclusion:The present study suggests that tempol may have antioxidant properties in LPS-induced liver injury. These results may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelated liver injury for further investigations.

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