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Oxidative stress plays important roles in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Tat-NR2B9c has shown efficacy as a neuroprotective agent in several studies. Here, we identified the neuroprotective role of Tat-NR2B9c after SAH and its related mechanisms. The results showed that Tat-NR2B9c treatment attenuated oxidative stress, therefore alleviated neuronal apoptosis and neurological deficits after SAH. Tat-NR2B9c treatment could alleviate mitochondrial vacuolization induced by SAH. Compared to SAH + vehicle group, Tat-NR2B9c resulted in the decrease of Acetylated superoxide dismutase2 (Ac-SOD2), Bcl-2-associated X protein (Bax) and cleaved-caspase3 (CC3) protein expression, and the up-regulation of Sirtunin 3 (Sirt3) and Bcl-2 protein level. Moreover, Tat-NR2B9c attenuated excitotoxicity by inhibiting the interaction of PSD95-NR2B-nNOS. Our results demonstrated that Tat-NR2B9c inhibited oxidative stress via inhibition of PSD95-NR2B-nNOS complex formation after SAH. Tat-NR2B9c may serve as a potential treatment for SAH induced brain injury., Competing Interests: Declaration of Competing interest None., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Stroke is the most common cerebrovascular disease and one of the leading causes of death and disability worldwide. The current conventional treatment for stroke involves increasing cerebral blood flow and reducing neuronal damage; however, there are no particularly effective therapeutic strategies for rehabilitation after neuronal damage. Therefore, there is an urgent need to identify a novel alternative therapy for stroke. Acupuncture has been applied in China for 3000 years and has been widely utilized in the treatment of cerebrovascular diseases. Accumulating evidence has revealed that acupuncture holds promise as a potential therapeutic strategy for stroke. In our present review, we focused on elucidating the possible mechanisms of acupuncture in the treatment of ischemic stroke, including nerve regeneration after brain injury, inhibition of inflammation, increased cerebral blood flow, and subsequent rehabilitation., Competing Interests: The authors declare no conflict of interest., (© 2024 The Author(s). Published by IMR Press.)

Subarachnoid hemorrhage (SAH) refers to vascular brain injury mainly from a ruptured aneurysm, which has a high lifetime risk and imposes a substantial burden on patients, families, and society. Previous studies on SAH mainly focused on neurons in gray matter (GM). However, according to literature reports in recent years, in-depth research on the mechanism of white matter (WM) is of great significance to injury and recovery after SAH. In terms of functional recovery after SAH, all kinds of cells in the central nervous system (CNS) should be protected. In other words, it is necessary to protect not only GM but also WM, not only neurons but also glial cells and axons, and not only for the lesion itself but also for the prevention and treatment of remote damage. Clarifying the mechanism of white matter injury (WMI) and repair after SAH is of great importance. Therefore, this present review systematically summarizes the current research on WMI after SAH, which might provide therapeutic targets for treatment after SAH., Competing Interests: The authors have declared that no competing interest exists., (Copyright © 2023 Yibo Liu et al.)

Spontaneous subarachnoid hemorrhage (SAH) accounts for 5-10% of all strokes and is a subtype of hemorrhagic stroke that places a heavy burden on health care. Despite great progress in surgical clipping and endovascular treatment for ruptured aneurysms, cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) threaten the long-term outcomes of patients with SAH. Moreover, there are limited drugs available to reduce the risk of DCI and adverse outcomes in SAH patients. New insight suggests that early brain injury (EBI), which occurs within 72 h after the onset of SAH, may lay the foundation for further DCI development and poor outcomes. The mechanisms of EBI mainly include excitotoxicity, oxidative stress, neuroinflammation, blood-brain barrier (BBB) destruction, and cellular death. Mitochondria are a double-membrane organelle, and they play an important role in energy production, cell growth, differentiation, apoptosis, and survival. Mitochondrial dysfunction, which can lead to mitochondrial membrane potential (Δψm) collapse, overproduction of reactive oxygen species (ROS), release of apoptogenic proteins, disorders of mitochondrial dynamics, and activation of mitochondria-related inflammation, is considered a novel mechanism of EBI related to DCI as well as post-SAH outcomes. In addition, mitophagy is activated after SAH. In this review, we discuss the latest perspectives on the role of mitochondria in EBI and DCI after SAH. We emphasize the potential of mitochondria as therapeutic targets and summarize the promising therapeutic strategies targeting mitochondria for SAH., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The caspase family is commonly involved in the pathophysiology of acute brain injury (ABI) through complex apoptotic, pyroptotic, and inflammatory pathways. Current translational strategies for caspase modulation in ABI primarily focus on caspase inhibitors. Because there are no caspase-inhibiting drugs approved for clinical use on the market, the development of caspase inhibitors remains an attractive challenge for researchers and clinicians. Therefore, we conducted the present review with the aim of providing a comprehensive introduction of caspases in ABI. In this review, we summarized the available evidence and potential mechanisms regarding the biological function of caspases. We also reviewed the therapeutic effects of caspase inhibitors on ABI and its subsequent complications. However, various important issues remain unclear, prompting further verification of the efficacy and safety regarding clinical application of caspase inhibitors. We believe that our work will be helpful to further understand the critical role of the caspase family and will provide novel therapeutic potential for ABI treatment., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Stroke is a disastrous neurological disease with high morbidity and mortality. The mechanism of the pathological process is extremely complicated and unclear. Although many basic studies have confirmed molecular mechanism of brain injury after stroke, these studies have not yet translated into treatment and clinical application. Ferroptosis is a form of cell death that is distinct from necrosis, apoptosis, and autophagy morphologically and biochemically and is characterized by iron‐dependent accumulation of lipid peroxides. Despite ferroptosis being first identified in cancer cells, it was recently revealed to also be a significant factor in the pathological process of stroke. A better understanding of ferroptosis in stroke may provide us with better therapeutic targets to treat this devastating disease. Here, we systematically summarized the current mechanism of ferroptosis and reviewed the current studies regarding the relationship between ferroptosis and stroke. [ABSTRACT FROM AUTHOR]