Showing 4 results for Birjandi
Mohtaram Yazdanian, Mahtab Moazami, Mohammad Shabani, Sadegh Cheragh Birjandi,
Volume 13, Issue 6 (Nov-Dec 2019)
Abstract
ABSTRACT
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
ABSTRACT
Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
Mohtaram Yazdanian, Mahtab Moazzami, Mohammad Shabani, Sadegh Cheragh Birjandi,
Volume 14, Issue 5 (Sep-Oct 2020)
Abstract
Background & Objective: Cerebral ischemia causes irreversible structural and functional damages in certain areas of the brain, especially the hippocampus. Evidence indicates that physical exercise may reduce the damages caused by cerebral ischemia. The purpose of this study was to examine the effect of 8-week exercise preconditioning on the expression of NT-3 and TrkC genes in the CA1 region of the hippocampus after the cerebral ischemic-reperfusion in male rats.
Methods: Twenty-one male Wistar rats weighing 250-300 gr were randomly selected and divided into three groups (healthy control, control + ischemia and exercise + ischemia). Rats in the exercise group ran on a treadmill 5 days per week for 8 weeks. Ischemia by occlusion of both common carotid arteries (CCA) was created for 45 minutes. In order to evaluate the gene expression, Real time PCR technique was used.
Findings: NT-3 gene expression was significantly different between exercise + ischemia with control + ischemia groups and control + ischemia with healthy control groups (P <0.05), and TrkC gene expression was significantly different between exercise + ischemia with healthy control groups and control + ischemia with healthy control groups (P <0.05).
Conclusion: The results of this study demonstrated that exercise before the induction of ischemic stroke increased the NT-3 gene expression but did not influence the TrKC gene expression.
Farnaz Aminian, Mahmood Hejazi, Sadegh Cheragh Birjandi,
Volume 14, Issue 5 (Sep-Oct 2020)
Abstract
Background and objectives: Evidence suggests that decrease in the serum concentration of myostatin (MSTN) may reduce age-related decrement in muscle mass, especially in older individuals. This study aimed at investigating the effects of 12 weeks of resistance training with and without blood flow restriction on MSTN and muscular strength (MS) of elderly women.
Methods: Thirty elderly women were randomly assigned into three groups of resistance training with blood flow restriction (n=10), resistance training without blood flow restriction (n=10) and control (n=10). The resistance training intervention was carried out three sessions a week for 12 weeks. Body composition, MS and serum concentrations MSTN were assessed at baseline and 48-36 hours after the last training session.
Results: There was a significant time × group difference in MS following 12 weeks of exercise intervention (P=0.001). However, there was no significant group and time × group difference in MSTN concentrations (P=0.2).
Conclusion: Low intensity BFRT does not decrease MSTN concentrations in elderly women. However, low intensity BFRT can increase MS values in these individuals.
Farnaz Aminian, Seyyed Mahmood Hejazi, Sadegh Cheragh Birjandi,
Volume 15, Issue 3 (May-Jun 2021)
Abstract
Background and objectives: Blood flow restriction training (BFRT) has gained substantial interest due to the lower required intensity, which may be beneficial for individuals who are not able to lift heavy weights. Therefore, we aimed at evaluating effects of 12 weeks of resistance training with and without blood flow restriction on follistatin (FST) concentrations and physical performance in elderly females.
Methods: Thirty elderly female were randomly assigned into the following groups: resistance training with blood flow restriction (BFRT; n=10), resistance training without blood flow restriction (WBFRT; n=10) and control ( n=10). The resistance training was carried out three session a week for 12 weeks. Serum concentrations of FST, muscular endurance and dynamic balance were assessed at baseline and after the 12week intervention.
Results: Significant main effects of time were observed for FST (p =0.03, η2 = 0.15), muscular endurance (p = 0.00, η2 = 0.59) and dynamic balance (p=0.00, η2 = 0.57). FST [BFRT= 1.4 ng/ml (effect size Cohen’s {d} = -0.8) significantly increased only in BFRT group. However, muscular endurance [BFRT= 95 (d= -4.1) and WBFRT = 32 (d= -0.9)] significantly increased in both intervention groups (P<0.05). In addition, dynamic balance [BFRT= -0.5 seconds (d= 2.2)] significantly increased only in the BFRT group (P<0.05).
Conclusion: BFRT was able to increase FST concentrations. Due to its mechanistic role in muscle mass alterations, elderly females can incorporate our BFRT protocol to improve anabolic conditions for muscular adaptations.
