ABSTRACT
Recent studies have shown that normobaric hyperoxia is effective in the treatment of acute ischemia, a phenomenon called preconditioning. However, the exact mechanism of this kind of preconditioning in vivo is not known. In this study, the effect of intermittent normobaric hyperoxia on expression of HIF1alpha in a stroke model was investigated. In this experimental study, rats were divided into 4 groups. Hyperoxia groups were exposed to 95% inspired oxygen for 4 h/day and 6 consecutive days. Oxygen concentration in the control groups was 21% [normoxia]. After 24 h, rats in stroke groups were subjected to 60 min of right middle cerebral artery occlusion. After 24 h, reperfusion neurological deficit scores were assessed. The brain HIF1alpha levels were analyzed by Western blot. Statistical analysis was performed using two-way ANOVA, Bonferroni post-test, Fisher exact test, and GraphPad Prism 5 software. The results of this study showed that HIF1alpha levels increased in stroke groups compared with normoxia groups, while the amount of protein in hyperoxia groups was not significantly different from normoxia groups. Significantly increased HIF1alpha levels were observed in hyperoxia stroke group. Also, hyperoxia improved neurological deficit scores from 8.83% down to 3.46%. Hydroxylation, instability, and degradation of HIF1alpha occurred following hyperoxia. In the stroke groups, lack of oxygen delivery to cells prevents hydroxylation and degradation of HIF1alpha. In hyperoxia stroke group, inflammatory cytokines with increased ROS can induce increased expression of HIF1alpha
ABSTRACT
The anabolic androgenic steroids are known to stimulate muscle protein synthesis and hypertrophy. Cardiomyocytes have two types of ATP-sensitive potassium channels in sarcolemma [sarck[ATP]] and in mitochondria [mitk[ATP]]. Activation of the sarck[ATP] channels has been proposed to protect against ischemia-reperfusion injury. This study aimed to investigate the effect of nandrolone decanoate [ND] on the expression of sarck[ATP] channels in the presence and absence of exercise in rat heart. In this experimental study, 40 adult male rats were divided into five groups: control, vehicle, ND, exercise and exercise-ND group. Rats in the exercise group were submitted to a running program on a treadmill, 5 days a week for 10 weeks. In addition, rats in the ND and exercise-ND groups received a weekly intramuscular injection of ND [10 mg/kg] for 10 weeks. Expression of the K[ATP] channel subunits [Kir6.2 and SUR2] was determined using the Western blotting method. ND administration had no effect on the expression of sarck[ATP] channel subunits in the sedentary group, while the chronic exercise significantly increased the expression of K[ATP] channel subunits [P=0.01]. Moreover, the ND administration significantly decreased the Kir6.2 [P=0.001] and SUR2 [P=0.05] subunits in the exercised animals. Chronic exercise and ND increases the expression of sarc[KATP] channels, and. The ND-induced expression decrement of channels is probably one of the mechanisms involved in the impairment of exercise-induced cardioprotection in rat heart