Department of Neuroscience and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.
Research Center of Psychiatry and Behavioral Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.
Cell Mol Neurobiol. 2023 Nov;43(8):3915-3928. doi: 10.1007/s10571-023-01413-w. Epub 2023 Sep 22.
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.
脑缺血及随后的再灌注导致特定脑区的血液供应减少，仍然是导致神经损伤、残疾和死亡的重要原因。在易损区域中，包括海马体在内的皮质下区域特别容易受到缺血性损伤，损伤的程度受到缺血不同阶段的影响。由于涉及自由基、氧化应激、炎症反应和谷氨酸毒性的复杂生化反应，神经组织会发生各种变化和损伤。这些过程的后果可能导致不可逆转的伤害。值得注意的是，自由基在缺血后的神经病理机制中起着关键作用，导致氧化应激。因此，缺血后抗氧化酶的功能对于防止氧化应激引起的海马损伤至关重要。本研究探讨了在缺血和再灌注的早期和晚期，海马神经元损伤和酶抗氧化活性。
