Mitophagy, the selective removal of damaged mitochondria through autophagy, is crucial for mitochondrial turnover and quality control. Docosahexaenoic acid (DHA), an essential omega‐3 fatty acid, protects mitochondria in various diseases. This study aimed to investigate the neuroprotective role of DHA in ischaemic stroke models in vitro and in vivo and its involvement in mitophagy and mitochondrial dysfunction. A mouse model of ischaemic stroke was established through middle cerebral artery occlusion (MCAO). To simulate ischaemic stroke in vitro, PC12 cells were subjected to oxygen–glucose deprivation (OGD). Immunofluorescence analysis, western blotting (WB), electron microscopy (EM), functional behavioural tests, and Seahorse assay were used for analysis. DHA treatment significantly alleviated the brain infarction volume, neuronal apoptosis, and behavioural dysfunction in mice with ischaemic stroke. In addition, DHA enhanced mitophagy by significantly increasing the number of autophagosomes and LC3‐positive mitochondria in neurons. The Seahorse assay revealed that DHA increased glutamate and succinate metabolism in neurons after ischaemic stroke. JC‐1 and MitoSox staining, and evaluation of ATP levels indicated that DHA‐induced mitophagy alleviated reactive oxygen species (ROS) accumulation and mitochondrial injury. Mechanistically, DHA improved mitochondrial dynamics by increasing the expression of dynamin‐related protein 1 (Drp1), LC3, and the mitophagy clearance protein Pink1/Parkin. Mdivi‐1, a specific mitophagy inhibitor, abrogated the neuroprotective effects of DHA, indicating that DHA protected neurons by enhancing mitophagy. Therefore, DHA can protect against neuronal apoptosis after stroke by clearing the damaged mitochondria through Pink1/Parkin‐mediated mitophagy and by alleviating mitochondrial dysfunction.

Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway.

Objective: Thalamic hemorrhage (TH) with hematoma extension into the brainstem can lead to poor outcomes. In this study, we discuss the feasibility of the endoscopic-assisted contralateral paramedian supracerebellar infratentorial (SCIT) approach as a therapeutic method for treating such patients.Case presentation: A patient suffered from a sudden loss of consciousness and right limb weakness, and a CT scan indicated TH with hematoma extension into the brainstem. She consented to undergo surgery by the endoscopic-assisted contralateral paramedian SCIT approach.Results: Now, the patient can open her eyes on her own and move her left arm in response to commands.Conclusion: The endoscopic-assisted contralateral paramedian SCIT approach may be a viable therapeutic method for treating TH patients with hematoma extension into the brainstem.

Contralateral sudden sensorineural hearing loss (SNHL) occurring after cerebellopontine surgery is rare [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17]. Presentation of petroclival meningioma followed by contralateral SNHL as a result of cerebellopontine surgery is quite uncommon, with only one case being previously reported [17]. Petroclival meningiomas are tumors containing dural attachments to the petroclival synchondrosis, typically near the upper two-thirds of the clivus, originating near the petroclival suture. Neighboring structures can be compromised, including the internal auditory meatus and Meckel cave, brainstem. Petroclinal meningiomas account for 2 % of all meningiomas [18]. Even though these tumors are slow growing, they can become quite large by the time symptoms arise. Subtotal resection can also lead to tumor recurrence. However, total resection poses a significant risk to the trochlear nerve if the tumor contains a supratentorial extension, especially when using the retrosigmoid approach. Centralis nerves 3, 5, 6 and 7 can be injured postoperatively. Contralateral SNHL would be detrimental to patients who have already experienced hearing loss due to petroclival meningiomas near the internal auditory meatus and can be injured after surgery. Thus, understanding the cause of contralateral SNHL and its treatment are both very critical. Here, we report and analyze this case to further elaborate on the causes of this rare, potentially catastrophic complication. Publication Date: 06 April 2021 (online) © 2021. Thieme. All rights reserved. Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany

Objective Interleukin-37 (IL-37), an anti-inflammatory cytokine within the interleukin-1 (IL-1) family, exhibits immunomodulatory properties. Here we evaluate the effects of IL-37 on microglia in neuroinflammation and its potential mechanisms. Methods C57BL/6 mice were injected intraperitoneally with 1 μg of recombinant human IL-37 protein (rhIL-37), and 24 h later with lipopolysaccharide (LPS) (5 mg/kg) to induce neuroinflammation. After 2-hour pretreatment of BV2 cells with rhIL-37 (100 ng/mL), an in vitro model was established by treating with LPS (100 ng/mL). Mice were assessed for behavioral tests, and neuronal damage was evaluated by Nissl staining and hematoxylin and eosin staining. The expression of Iba1, CD86, CD206, and NF-κB were detected by immunofluorescence staining, and inflammatory mediators and pathway proteins were evaluated by ELISA, qRT-PCR, and Western blot. Results IL-37 significantly ameliorated LPS-induced behavioral deficits and protected mice from inflammatory injury. In vitro experiments suggested that IL-37 modulates polarization of microglia from M1 to M2 phenotype, along with reducing pro-inflammatory cytokine production. Moreover, IL-37 attenuated the production of NF-κB and MyD88. Conclusions IL-37 regulates microglia against neuroinflammatory responses by blocking the MyD88/NF-κB pathway and shows for the first time how IL-37 influences the phenotype of microglia, suggesting a potential therapeutic target for neuroinflammation.