Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Clinical Research Center for Neurological Diseases of Zhejiang Province, Hangzhou, China.
CNS Neurosci Ther. 2023 Dec;29(12):3672-3683. doi: 10.1111/cns.14348. Epub 2023 Jul 5.
Spontaneous subarachnoid hemorrhage (SAH) is one of the most devastating forms of stroke, with limited treatment modalities and poor patient outcomes. Previous studies have proposed multiple prognostic factors; however, relative research on treatment has not yet yielded favorable clinical outcomes. Moreover, recent studies have suggested that early brain injury (EBI) occurring within 72 h after SAH may contribute to its poor clinical outcomes. Oxidative stress is recognized as one of the main mechanisms of EBI, which causes damage to various subcellular organelles, including the mitochondria, nucleus, endoplasmic reticulum (ER), and lysosomes. This could lead to significant impairment of numerous cellular functions, such as energy supply, protein synthesis, and autophagy, which may directly contribute to the development of EBI and poor long-term prognostic outcomes. In this review, the mechanisms underlying the connection between oxidative stress and subcellular organelles after SAH are discussed, and promising therapeutic options based on these mechanisms are summarized.
自发性蛛网膜下腔出血（SAH）是最具破坏性的中风类型之一，治疗方法有限，患者预后较差。既往研究提出了多种预后因素；然而，关于治疗的相关研究尚未产生有利的临床结果。此外，最近的研究表明，SAH 后 72 小时内发生的早期脑损伤（EBI）可能导致其临床预后不良。氧化应激被认为是 EBI 的主要机制之一，它会导致包括线粒体、细胞核、内质网（ER）和溶酶体在内的各种亚细胞细胞器受损。这可能导致许多细胞功能严重受损，如能量供应、蛋白质合成和自噬，这可能直接导致 EBI 的发展和不良的长期预后结果。在这篇综述中，讨论了 SAH 后氧化应激与亚细胞细胞器之间联系的机制，并总结了基于这些机制的有前途的治疗选择。
