Mitochondrial dysfunction is considered a crucial therapeutic target for early brain injury following subarachnoid hemorrhage (SAH). Emerging evidence indicates that docosahexaenoic acid (DHA), an essential omega-3 fatty acid, protects mitochondria in various chronic diseases. This study aimed to investigate the neuroprotective effects of DHA on mitochondrial dynamic dysfunction after EBI using in vivo and in vitro approaches. For in vivo experiments, the rat endovascular perforation SAH model was performed, whereby DHA was administered intravenously 1 h after induction of SAH. Primary cultured neurons treated with oxyhemoglobin (OxyHb) for 24 h were used to mimic SAH in vitro. Our results demonstrated that DHA improved neurological deficits and reduced brain edema in rats with SAH, and attenuated OxyHb-induced neuronal death in primary cultured cells. DHA reduced the amount of reactive oxygen species-positive cells and improved cell viability when compared to the SAH + vehicle group in vitro. DHA attenuated malondialdehyde levels and superoxide dismutase stress, increased Bcl2 and Bcl-xl, and decreased Bax and cleaved caspase-3 in vivo. Additionally, DHA ameliorated mitochondrial dysfunction, upregulated the mitochondrial fusion-related protein Optic Atrophy 1, and downregulated the mitochondrial fission-related protein Dynamin-Related-Protein 1 (Drp1) and Serine 616 phosphorylated Drp1 after SAH both in vitro and in vivo. Taken together, our current study demonstrates that DHA might prevent oxidative stress-based apoptosis after SAH. The characterization of the underlying molecular mechanisms may further improve mitochondrial dynamics-related signaling pathways.

Mdivi-1 is a selective inhibitor of mitochondrial fission protein, Drp1, and can penetrate the blood-brain barrier. Previous studies have shown that Mdivi-1 improves neurological outcomes after ischemia, seizures and trauma but it remains unclear whether Mdivi-1 can attenuate early brain injury after subarachnoid hemorrhage (SAH). We thus investigated the therapeutic effect of Mdivi-1 on early brain injury following SAH. Rats were randomly divided into four groups: sham; SAH; SAH + vehicle; and SAH + Mdivi-1. The SAH model was induced by standard intravascular perforation and all of the rats were subsequently sacrificed 24 h after SAH. Mdivi-1 (1.2 mg/kg) was administered to rats 30 min after SAH. We found that Mdivi-1 markedly improved neurologic deficits, alleviated brain edema and BBB permeability, and attenuated apoptotic cell death. Mdivi-1 also significantly reduced the expression of cleaved caspase-3, Drp1 and p-Drp1, attenuated the release of Cytochrome C from mitochondria, inhibited excessive mitochondrial fission, and restored the ultra-structure of mitochondria. Furthermore, Mdivi-1 reduced levels of MDA, 3-NT, and 8-OHdG, and improved SOD activity. Taken together, our data suggest that Mdivi-1 exerts neuroprotective effects against cell death induced by SAH and the underlying mechanism may be inhibition of Drp1-activated mitochondrial fission and oxidative stress.

The treatment of brain arteriovenous malformations (AVMs) remains a significant challenge, especially hemorrhagic AVMs which are unsuitable for microsurgery or radiosurgery. We demonstrate an AVM located in the left basal ganglia area, supplied by slender arteries, and treated by the transvenous pressure cooker technique. Herein, we describe the procedure and outline the crucial points and indications for this technique.

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Purpose. Using retinal optical coherence tomography angiography (OCTA), we aimed to investigate the changes in important indicators of cerebral microcirculatory disorders, such as the properties of the radial peripapillary capillaries, vascular complexes, and the retinal nerve fiber layer, caused by carotid stenosis and postoperative reperfusion. Methods. In this prospective longitudinal cohort study, we recruited 40 carotid stenosis patients and 89 healthy volunteers in the First Affiliated Hospital of Harbin Medical University (Harbin, China). Eyes with ipsilateral carotid stenosis constituted the experimental group, while the fellow eyes constituted the contralateral eye group. Digital subtraction angiography, CT perfusion imaging (CTP), and OCTA examinations were performed in all subjects. The vessel density of the radial peripapillary capillaries (RPC), superficial retinal vascular complexes (SVC), deep vascular complexes (DVC), choriocapillaris (CC), and the thickness of the retinal nerve fiber layer (RNFL) were assessed. Propensity-matched analysis was undertaken to adjust for covariate imbalances. Intergroup comparative analysis was conducted, and the paired sample t -test was used to evaluate the preoperative and postoperative changes in OCTA variables. Results. The ocular vessel density in the experimental group was significantly lower than that in the control group (RPC: 55.95 vs. 57.24, P = 0.0161 ; SVC: 48.65 vs. 52.22, P = 0.0006 ; DVC: 49.65 vs. 57.50, P < 0.0001 ). Participants with severe carotid stenosis have reduced contralateral ocular vessel density (RPC 54.30; SVC 48.50; DVC 50.80). Unilateral stenosis removal resulted in an increase in vessel density on both sides, which was detected by OCTA on the 4th day (RPC, P < 0.0001 ; SVC, P = 0.0104 ; DVC, P = 0.0104 ). Moreover, the ocular perfusion was consistent with that established by CTP. Conclusion. OCTA can be used for sensitive detection and accurate evaluation of decreased ocular perfusion caused by carotid stenosis and may thus have the potential for application in noninvasive detection of cerebral microcirculation disorders. This trial is registered with NCT04326842.