2nd International Conference on Dementia and Brain Disorders & 3rd International Conference on Neurology & Neurological Disorders
November 06-07, 2025 | London, UK
Alieh Bashghareh
Shahroud university of medical scineces, Iran
Ischemia/reperfusion (I/R) injury initiates a complex cascade of pathological events in the hippocampus, including widespread neuronal loss, activation of inflammatory pathways, significant suppression of antioxidant defense systems, and alterations in the expression of brain-derived neurotrophic factor (BDNF). However, the exact pattern of BDNF expression changes across different time points following I/R injury remains unclear. Adult male rats underwent I/R surgery using a bilateral common carotid artery occlusion model, followed by reperfusion periods of 6 hours, 12 hours, 2 days, 5 days, and 7 days. BDNF expression levels and superoxide dismutase (SOD) activity were assessed using ELISA, neuronal damage was evaluated by Nissl staining, and tumor necrosis factor-alpha (TNF-α) expression was assessed immunohistochemically. This study observed significant neuronal damage in the hippocampal CA1 region, characterized by increased dark neuron counts, which peaked at 12 hours post-ischemia. Concurrently, BDNF expression was significantly reduced at 12 hours and 5 days post-ischemia, with notable decreases also observed at 2 and 7 days. Conversely, TNF-α levels showed a significant increase at 6 and 12 hours and 5 days post-ischemia, indicating a biphasic inflammatory response. Furthermore, SOD activity was significantly decreased across all ischemic groups compared to the sham group, highlighting a compromised antioxidant defense. Our findings reveal a critical temporal cascade following I/R injury, characterized by early neuronal damage, dynamic BDNF modulation, and biphasic inflammation. A reduction in BDNF, accompanied by increased TNF-α and decreased SOD, underscores the connection between oxidative stress, inflammation, and neurotrophic support in ischemic brain injury. This study highlights the potential for strategies that target early oxidative stress and sustained inflammation to preserve BDNF and enhance stroke recovery outcomes.
Keywords: Ischemia/reperfusion injury, BDNF, TNF-α, hippocampus, Different time points
Alieh Bashghareh is a dedicated researcher and faculty member at Shahroud University of Medical Sciences in Shahroud, Iran. With a strong academic background in medical sciences, she is actively involved in research, education, and community health advancement. Dr. Bashghareh’s work focuses on improving healthcare outcomes through evidence-based practices and interdisciplinary collaboration. Her commitment to scientific excellence and education contributes significantly to the academic and research mission of Shahroud University of Medical Sciences