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2.
Exp Ther Med ; 14(5): 3961-3970, 2017 Nov.
Article in English | MEDLINE | ID: mdl-29067093

ABSTRACT

The present study reports the effect of successful treatment of cerebral venous sinus thrombosis (CVST) with stent retriever thrombectomy combined with local thrombolytic therapy. Medical records of 29 patients were retrospectively analyzed following a diagnosis of CVST with magnetic resonance venography (MRV) or digital subtraction angiography (DSA). Systemic anticoagulation was the initial treatment in all patients following admission. In group A, stent retriever thrombectomy combined with local thrombolytic therapy was performed on 14 patients who met the criteria of endovascular therapy. Stent-assisted angioplasty was also performed when patients presented with venous sinus stenosis. A total of 15 patients in group B received systemic anticoagulant treatment. Subsequently, warfarin was administered orally for 3 to 12 months as a continuous anticoagulant therapy. International normalized ratio was monitored when patients were receiving anticoagulant therapy. Additionally, clinical presentation, decision to escalate therapy, recanalization, Glasgow Coma Scale, modified Rankin Scale (mRS) and the clinical outcome was assessed. A total of 14 patients (9 female patients, 5 male patients), with ages ranging from 17 to 57 years, met the criteria of endovascular therapy. The clinical symptoms of 12 patients had improved after receiving endovascular therapy and only 2 patients suffered from intracranial hemorrhage following the procedure. Complete recanalization of venous sinus was exhibited in 10/14 (71.4%) patients in group A when compared with 1/15 (6.7%) patients in group B. mRS were improved in the 12-month follow-up in groups A and B when compared with that at admission. In the present study, patients with acute CVST treated with stent retriever thrombectomy combined with local thrombolytic therapy had a favorable outcome. To conclude, the present study provides a treatment option in treating CVST, particularly for patients that present with evident cortical venous outflow stasis or deteriorate neurology, despite appropriate anticoagulant therapy.

3.
Neurochem Res ; 41(11): 3095-3102, 2016 Nov.
Article in English | MEDLINE | ID: mdl-27518088

ABSTRACT

Previous studies have demonstrated that baicalein has protective effects against several diseases, which including ischemic stroke. The effect of baicalein on the blood-brain barrier (BBB) in intracerebral hemorrhage (ICH) and its related mechanisms are not well understood. We aimed to investigate the mechanisms by which baicalein may influence the BBB in a rat model of ICH. The rat model of ICH was induced by intravenous injection of collagenase IV into the brain. Animals were randomly divided into three groups: sham operation, vehicle, and baicalein group. Each group was then divided into subgroups, in which the rats were sacrificed at 24 and 72 h after ICH. We assessed brain edema, behavioral changes, BBB leakage, apoptosis, inducible nitric oxide synthase (iNOS), zonula occludens (ZO)-1, Mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). Treatment with baicalein reduced brain water content, BBB leakage, apoptosis, and neurologic deficits, compared with vehicle. Baicalein also decreased ICH-induced changes in the levels of iNOS but increased the levels of ZO-1. The protective effect of baicalein on the BBB in ICH rats was possibly invoked by attenuated p-38 MAPK and JNK phosphorylation, and decreased activation of the NF-κB signaling pathway, which may have suppressed gene transcription, including iNOS, and eventually decreased formation of peroxynitrite (ONOO-). Our results suggest that baicalein exerts a protective effect on BBB disruption in the rat model of ICH. The likely mechanism is via inhibition of MAPKs and NF-κB signaling pathways, leading to decreased formation of iNOS and ONOO-, thereby improving neurological function.


Subject(s)
Blood-Brain Barrier/drug effects , Cerebral Hemorrhage/drug therapy , Flavanones/pharmacology , Animals , Biological Transport/drug effects , Brain Edema/drug therapy , Brain Edema/metabolism , Cerebral Hemorrhage/metabolism , Disease Models, Animal , MAP Kinase Signaling System/drug effects , Male , Mitogen-Activated Protein Kinases/metabolism , Rats, Sprague-Dawley
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