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    Activation of BDNF- and VEGF-mediated Neuroprotection by Treadmill Exercise Training in Experimental Stroke
    (Springer/Plenum Publishers, 2022) Sayyah, Mansour; Seydyousefi, Mehdi; Moghanlou, Abdorreza Eghbal; Metz, Gerlinde A. S.; Shamsaei, Nabi; Faghfoori, Mohammad Hasan; Faghfoori, Zeinab
    Early treatment of ischemic stroke is one of the most effective ways to reduce brains' cell death and promote functional recovery. This study was designed to examine the effect of aerobic exercise on post ischemia/reperfusion injury on concentration and expression of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) after inducing a neuronal loss in CA1 region of hippocampus in Male Wistar rats. Three experimental groups including sham(S), ischemia/reperfusion-control (IRC) and ischemia/reperfusion exercise (IRE) were used for this purpose. The rats in the IRE group received a bilateral carotid artery occlusion treatment. They ran for 45 minutes on a treadmill five days per week for eight consecutive weeks. Cresyl violet (Nissl), Hematoxylin (H & E) and Eosin staining procedure were used to determine the extent of damage. A ladder rung walking task was used to assess the functional impairments and recovery after the ischemic lesion. ELISA and immunohistochemistry method were employed to measure BDNF and VEGF protein expressions. The result showed that the brain ischemia/reperfusion condition increased the cell death in hippocampal CA1 neurons and impaired motor performance on the ladder rung task whereas the aerobic exercise program significantly decreased the brain cell's death and improved motor skill performance. It was concluded that ischemic brain lesion decreased the BDNF and VEGF expression. It seems that the aerobic exercise following the ischemia/reperfusion potentially promotes neuroprotective mechanisms and neuronal repair and survival mediated partly by BDNF and other pathways.
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    Endurance Training and Exogenous Adenosine Infusion Mitigate Hippocampal Inflammation and Cell Death in a Rat Model of Cerebral Ischemia/Reperfusion Injury: A Randomized Controlled Trial
    (Briefland, 2022) Eslami, Zahra; Ghomi, Masoumeh Rezaei; Saidi, Aref; Mousavi, Seyedeh Vafa; Farhadi, Mahboubeh; Robati, Najmeh Sheikh; Moghanlou, Abdorreza Eghbal
    Background: Cerebral ischemia can cause irreversible structural and functional damages to the brain, especially to the hippocampus. Preconditioning with endurance training and endogenous adenosine infusion may reduce ischemia-associated damages. Objectives: This study aimed to evaluate the effect of preconditioning with endurance training and endogenous adenosine infusion on cell death in the hippocampal CA1 region following ischemia/reperfusion injuries in a rat model. Methods: Male Wistar rats were divided into five groups: (1) control (n = 8); (2) ischemia (n =12); (3) endurance training + ischemia (n = 12); (4) adenosine infusion + ischemia (n =12); and (5) endurance training + adenosine infusion + ischemia (n =12). The rats in the training groups ran on a treadmill five days per week for eight weeks. In the adenosine infusion groups, the rats were injected 0.1 mg/mL/kg of adenosine intraperitoneally. Also, in the ischemic groups, both common carotid arteries were clamped for 45 minutes. Cresyl violet staining and real-time polymerase chain reaction (PCR) assay were used to evaluate cell death and cytokine gene expression, respectively. Results: Based on the present results, treatments, including endurance training + ischemia, adenosine infusion + ischemia, and endurance training + adenosine infusion + ischemia reduced the level of interleukin-6 (IL-6) and glutamate gene expression, respectively, compared to the group of ischemia only. In contrast, the expression of nerve growth factor (NGF) and adenosine receptor (A2A) genes increased by seven, four, and two folds in the endurance training + ischemia, adenosine infusion + ischemia, and endurance training + adenosine infusion + ischemia groups, respectively, compared to the group of ischemia only. Conclusions: Endurance training on a treadmill and exogenous adenosine infusion synergistically diminished cell death and reduced the expression of pro-inflammatory cytokines, while promoting the neurotrophic factor expression. When endurance training and adenosine infusion were used as stimulants before the induction of cerebral ischemia, they significantly reduced cell death.
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    Habitual Caffeine Consumption and Training Status Affect the Ergogenicity of Acute Caffeine Intake on Exercise Performance
    (Sage Publications Inc, 2025) Khodadadi, Davar; Azimi, Farhad; Moghanlou, Abdorreza Eghbal; Gursoy, Recep; Demirli, Abdullah; Jalali, Parham; Behdari, Reza
    Background: Acute caffeine ingestion can improve exercise performance. Interplay between caffeine habituation and training status on the performance-enhancing effect of caffeine is unknown. Hypothesis: Habitual caffeine consumption and training status affect the ergogenicity of pre-exercise caffeine intake on exercise performance. Study Design: Double-blind, placebo-controlled, counterbalanced experimental design. Level of Evidence: Level 3. Methods: Eighty physically inactive men were randomized into 1 of 4 groups: caffeine supplementation (CAF), caffeine supplementation + exercise training (CAFEXE), placebo (PLA), and placebo + exercise training (PLAEXE); high-intensity interval training and caffeine were administered for 9 and 8 weeks, respectively. Data were collected pre-test, mid-test, post-test, and delayed post-test, each including 2 experiment sessions (3 mg/kg caffeine or placebo), with an additional experiment session post-test (6 mg/kg caffeine). In each experiment session, 45-min after consuming a placebo or caffeine, a 3-km running test and a Wingate power test were performed. Results: Pre-exercise ingestion of 3 mg/kg caffeine improved 3-km running time and mean power output (MPO) in all groups at all stages (P < 0.05); this effect was higher in trained than in untrained volunteers (P < 0.05). Habitual caffeine consumption reduced the ergogenic effect of caffeine in both aerobic and anaerobic trials (P < 0.05); 6 mg/kg caffeine enhanced this decrease only in CAFEXE (P < 0.05). Short-term caffeine withdrawal augmented the reduced ergogenic effect of caffeine on 3-km running performance and MPO in CAF and CAFEXE (P < 0.05). Conclusion: Habituation to caffeine and training status could partially influence the ergogenic effects of caffeine on exercise performance.
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    Neuroprotective effects of pre-ischemic exercise are linked to expression of NT-3/NT-4 and TrkB/TrkC in rats
    (Pergamon-Elsevier Science Ltd, 2023) Moghanlou, Abdorreza Eghbal; Yazdanian, Mohtaram; Roshani, Sajad; Demirli, Abdullah; Seydyousefi, Mehdi; Metz, Gerlinde A. S.; Faghfoori, Zeinab
    Introduction and objective: Stroke causes irreversible damage, particularly to the hippocampus. Evidence suggests that exercise training may mitigate adverse structural and functional consequences of an ischemic lesion in the brain. The purpose of this study was to investigate the effects of preconditioning exercise on expression of neurotrophic factor genes and proteins in hippocampalCA1 region and their relationship with sensorimotor recovery following global ischemia/reperfusion (Is/Re) injury in a rat model of stroke.Methods: Male Wistar rats were randomly assigned to Exercise+Ischemia/Reperfusion (Ex+Is/Re),Con-trol+Ischemia/Reperfusion (Co+Is/Re), and Sham treatments. Rats in the exercise groups ran on a treadmill for 45 min/d for five days/week for 8 consecutive weeks prior to Is/Re lesion.Ischemia was induced by common carotid artery occlusion (CCAO). The ladder rung walking task was used to assess functional impairments and recovery following ischemic lesion.Tissue from hippocampal area CA1 was inspected for ischemia-induced cell loss and gene and protein expression linked to neurotrophins NT-3, NT-4, and their receptorsTrkB and TrkC. Results: CCAO caused hippocampal cell death in CA1 and resulted in significant sensori motor impairments in the ladder rung walking task. In contrast, pre-ischemic exercise considerably reduced cell death and supported sensorimotor recovery following CCAO.In addition, NT-3, NT-4,TrkB and TrkC gene expression and their protein levels were significantly increased inthe Ex+Is/Re group compared to Co+Is/Re (p < 0.05).Conclusion: The findings showed that pre-ischemic exercise can exert neuroprotective effects via NT-3 and NT-4 pathways against ischemia in hippocampal CA1 neurons and promote post-injury sensorimotor recovery.