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Mohtaram Yazdanian, Mahtab Moazami, Mohammad Shabani, Sadegh Cheragh Birjandi,
Volume 13, Issue 6 (11-2019)
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.

Parisa Zeinali, Marie Saghaeian, Jahanbakhsh Asadi, Seyyed Mehdi Jafari,
Volume 16, Issue 5 (9-2022)
Abstract

Background and objectives: Activation of adenosine A2a receptor has been shown to induce the growth and metastasis of cancer cells. The role of this receptor in esophageal cancer has not yet been determined. The present study aimed to investigate effects of an adenosine A2a receptor antagonist (3, 7-dimethyl-1-propargylxanthine) on growth of esophageal cancer cells.
Methods: Real-time polymerase chain reaction was performed to evaluate mRNA expression of the A2a adenosine receptor in KYSE-30 and YM-1 esophageal cancer cell lines. Effects of the antagonist on viability of the cells were evaluated by MTT assay.
Results: At low concentrations, the antagonist had no effect on cell viability. However, at concentrations ≥200 μM, the antagonist significantly reduced viability of both cell lines (p<0.05).
Conclusion: The results of this study indicate that the adenosine A2a receptor antagonist exerts inhibitory effects on KYSE30 and YM-1 cancer cells in a dose-dependent manner. Therefore, the use of this antagonist can be exploited as a therapeutic target for the treatment of esophageal cancer.

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