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Background: Mesenchymal stem cells (MSCs) are suspected to exert neuroprotective effects in brain injury, in part through the secretion of extracellular vesicles like exosomes containing bioactive compounds. We now investigate the mechanism by which bone marrow MSCs (BMSCs)-derived exosomes harboring the small non-coding RNA miR-29b-3p protect against hypoxic-ischemic brain injury in rats. Methods:We established a rat model of middle cerebral artery occlusion (MCAO) and primary cortical neuron or brain microvascular endothelial cell (BMEC) models of oxygen and glucose deprivation (OGD). Exosomes were isolated from the culture medium of BMSCs. We treated the MCAO rats with BMSC-derived exosomes in vivo, and likewise the OGD-treated neurons and BMECs in vitro. We then measured apoptosis-and angiogenesis-related features using TUNEL and CD31 immunohistochemical staining and in vitro Matrigel angiogenesis assays. Results: The dual luciferase reporter gene assay showed that miR-29b-3p targeted the protein phosphatase and tensin homolog (PTEN). miR-29b-3p was downregulated and PTEN was upregulated in the brain of MCAO rats and in OGD-treated cultured neurons. MCAO rats and OGD-treated neurons showed promoted apoptosis and decreased angiogenesis, but overexpression of miR-29b-3p or silencing of PTEN could reverse these alterations. Furthermore, miR-29b-3p could negatively regulate PTEN and activate the Akt signaling pathway. BMSCs-derived exosomes also exerted protective effects against apoptosis of OGD neurons and cell apoptosis in the brain samples from MCAO rats, where we also observed promotion of angiogenesis.Conclusion: BMSC-derived exosomal miR-29b-3p ameliorates ischemic brain injury by promoting angiogenesis and suppressing neuronal apoptosis, a finding which may be of great significance in the treatment of hypoxic-ischemic brain injury.

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A cavernous sinus dural arteriovenous fistula (CS-DAVF) is an abnormal arteriovenous communication involving the dura mater within or near the CS wall. The dural arteries from the internal carotid artery and external carotid artery supply the CS-DAVF, and the superior ophthalmic vein (SOV) and inferior petrous sinus (IPS) are frequent venous drainers. In CS-DAVF cases, high-risk lesions require treatment. Endovascular treatment (EVT) has been the first-line option for CS-DAVFs. To our knowledge, a review of the EVT of CS-DAVFs is lacking. Therefore, in this paper, we review the available literature on this issue. In addition, some illustrative cases are also provided to more concisely expound the EVT of CS-DAVFs. According to the recent literature, transvenous embolization via the IPS is considered the most effective method for EVT of CS-DAVFs. In addition, the transorbital approach is another reasonable choice. Other venous approaches can also be tried. Because of the low cure rate, transarterial embolization for CS-DAVFs is limited to only highly selected patients. In the EVT of CS-DAVFs, various agents have been used, including coil, Onyx, and n-butyl cyanoacrylate, with coil being the preferred one. In addition, when EVT cannot obliterate the CS-DAVF, stereotactic radiotherapy may be considered. In general, despite various complications, EVT is a feasible and effective method to manage CS-DAVFs by way of various access routes and can yield a good prognosis.

Background Though flow diverter is a safe and efficient modality, some patients can experience delayed aneurysmal rupture. The mechanism of delayed rupture is still obscure to us. Methods We performed a systematic search in the PubMed database for patients with delayed rupture of intracranial aneurysms after flow diverter placement. Results A total of 36 articles reporting on 60 patients were included in the final analysis. Of the 49 patients with description of presenting symptoms, six (12.2%) patients were incidentally diagnosed, 39 (87.8%) patients were admitted for aneurysmal rupture or mass effect. Multiple flow diverters were used in 38.3% (18/47) of the patients. Coil assistance was applied in 13.0% (7/54) of the patients. Delayed aneurysmal rupture led to intracranial hemorrhage or carotid–cavernous sinus fistula (CCF) in 76.8% (43/56) and 23.2% (13/56) of the patients, respectively. Of the 55 patients with description of outcome, 14 (25.5%) patients achieved good recovery, one (1.8%) patient was severely disabled, 40 (72.7%) patients died. All of the patients in the CCF group survived and experienced good recovery. Conclusion Increased intra-aneurysmal pressure, destabilization of the aneurysm wall by intra-aneurysmal thrombus, persistent residual intra-aneurysmal flow, characteristics of the specific aneurysm, and mechanical injury by the flow diverter might conjointly contribute to the final delayed rupture. There has been no established preventive measure to decrease the incidence of delayed rupture yet. The treatment and outcome depend on the presentation of delayed rupture. Patients presenting with aneurysm-related intracranial hemorrhage have a dismal outcome. Those presenting with CCFs usually have a satisfactory recovery.

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