The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus

Abstract

Cerebral ischemia and subsequent reperfusion, leading to reduced blood supply to specific brain areas, remain significant contributors to neurological damage, disability, and mortality. Among the vulnerable regions, the subcortical areas, including the hippocampus, are particularly susceptible to ischemia-induced injuries, with the extent of damage influenced by the different stages of ischemia. Neural tissue undergoes various changes and damage due to intricate biochemical reactions involving free radicals, oxidative stress, inflammatory responses, and glutamate toxicity. The consequences of these processes can result in irreversible harm. Notably, free radicals play a pivotal role in the neuropathological mechanisms following ischemia, contributing to oxidative stress. Therefore, the function of antioxidant enzymes after ischemia becomes crucial in preventing hippocampal damage caused by oxidative stress. This study explores hippocampal neuronal damage and enzymatic antioxidant activity during ischemia and reperfusion's early and late stages.

Keywords: Antioxidant enzymes; Cerebral ischemia; Hippocampus; Neuronal damage; Oxidative stress.

Fig. 1

Enzymatic antioxidant levels and hippocampal neuronal damage during early and late stages of ischemia

Fig. 2

Disruption in the balance between oxidative stress production and the enzymatic antioxidant system due to cerebral ischemia and its impact on neural damage and cognitive impairment

Fig. 3

Molecular ischemia mechanisms at synaptic levels and the resulting neuronal effects in early and late stages