Kim Sehwan, Jung Un Ju, Kim Sang Ryong
School of Life Science and Biotechnology, Kyungpook National University, Daegu 41566, Republic of Korea.
BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea.
Antioxidants (Basel). 2024 Nov 28;13(12):1462. doi: 10.3390/antiox13121462.
Upregulation of reactive oxygen species (ROS) levels is a principal feature observed in the brains of neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD). In these diseases, oxidative stress can disrupt the blood-brain barrier (BBB). This disruption allows neurotoxic plasma components, blood cells, and pathogens to enter the brain, leading to increased ROS production, mitochondrial dysfunction, and inflammation. Collectively, these factors result in protein modification, lipid peroxidation, DNA damage, and, ultimately, neural cell damage. In this review article, we present the mechanisms by which oxidative damage leads to BBB breakdown in brain diseases. Additionally, we summarize potential therapeutic approaches aimed at reducing oxidative damage that contributes to BBB disruption in neurodegenerative diseases.
活性氧(ROS)水平上调是在帕金森病(PD)和阿尔茨海默病(AD)等神经退行性疾病的大脑中观察到的一个主要特征。在这些疾病中,氧化应激会破坏血脑屏障(BBB)。这种破坏使神经毒性血浆成分、血细胞和病原体进入大脑,导致ROS产生增加、线粒体功能障碍和炎症。总的来说,这些因素会导致蛋白质修饰、脂质过氧化、DNA损伤,并最终导致神经细胞损伤。在这篇综述文章中,我们阐述了氧化损伤导致脑部疾病中血脑屏障破坏的机制。此外,我们总结了旨在减少导致神经退行性疾病中血脑屏障破坏的氧化损伤的潜在治疗方法。