Long-Term Stress-Induced Neurological Deficits In Hippocampal Tissue Of Animals Following Stroke

Objective: Ischemic stroke being the most prevalent type of stroke, affecting the vulnerable hippocampus. Understanding the interplay between long-term stress and stroke-related cognitive dysfunction is crucial, as chronic stress exacerbates oxidative damage and may hinder recovery. Therefore, this study aimed to investigate the levels of oxidative stress in hippocampal tissue following long-term stress exposure in a rat model post-stroke. Methods: This study utilized ۲۴ male rats. The rats were randomly assigned to four groups: a sham group, a long-term stress model (LSM) group, a control group (stroke induction), and a long-term stress with stroke induction (LSC) group. The long-term stress protocol involved daily immobilization in transparent plexiglass restrainers for four hours over ۱۵ consecutive days. Following ۲۱ days post-surgery, biochemical assessments included measuring malondialdehyde (MDA) levels using a thiobarbituric acid assay and total thiol (-SH) concentrations in the hippocampus using the DTNB reagent. Results: The control, LSM, and LSC groups exhibited significantly higher MDA levels compared to the sham group (p<۰.۰۱). Conversely, -SH levels were significantly elevated in the control and LSC groups compared to the sham group, while the LSM group showed no notable changes in -SH levels. ANOVA results confirmed that both MDA and -SH concentrations were significantly influenced by the interventions (p = ۰.۰۰۱۳ and p = ۰.۰۰۳۲, respectively). Conclusion: This study highlights the significant interplay between long-term stress and oxidative damage in the context of stroke, emphasizing the necessity for integrated therapeutic strategies that address both psychological and physiological recovery.

کلیدواژه ها:

Intracerebral haemorrhage ، Oxidative stress ، Lipid peroxidation ، Striatum