9 research outputs found
Factors associated with post-stroke depression and fatigue: lesion location and coping styles
Retraction Note to: Factors associated with post-stroke depression and fatigue: lesion location and coping styles
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Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models
Background: Evidence suggests that brain infiltration of lymphocytes contributes to acute neural injury after cerebral ischemia. However, the spatio-temporal dynamics of brain-infiltrating lymphocytes during the late stage after cerebral ischemia remains unclear. Methods: C57BL/6 (B6) mice were subjected to sham, photothrombosis, or 60-min transient middle cerebral artery occlusion (MCAO) procedures. Infarct volume, neurodeficits, production of reactive oxygen species (ROS) and inflammatory factors, brain-infiltrating lymphocytes, and their activation as well as pro-inflammatory cytokine IFN-γ production were assessed. Brain-infiltrating lymphocytes were also measured in tissue sections from post-mortem patients after ischemic stroke by immunostaining. Results: In mice subjected to transient MCAO or photothrombotic stroke, we found that lymphocyte infiltration persists in the ischemic brain until at least day 14 after surgery, during which brain infarct volume significantly diminished. These brain-infiltrating lymphocytes express activation marker CD69 and produce proinflammatory cytokines such as IFN-γ, accompanied with a sustained increase of reactive oxygen species (ROS) and inflammatory cytokines release in the brain. In addition, brain-infiltrating lymphocytes were observed in post-mortem brain sections from patients during the late stage of ischemic stroke. Conclusion: Our results demonstrate that brain-infiltration of lymphocytes persists after the acute stage of cerebral ischemia, facilitating future advanced studies to reveal the precise role of lymphocytes during late stage of stroke. Electronic supplementary material The online version of this article (10.1186/s12974-017-1017-0) contains supplementary material, which is available to authorized users
Vinpocetine Inhibits NF-κB-Dependent Inflammation in Acute Ischemic Stroke Patients
Immunity and inflammation play critical roles in the pathogenesis of acute ischemic stroke. Therefore, immune intervention, as a new therapeutic strategy, is worthy of exploration. Here, we tested the inflammation modulator, vinpocetine, for its effect on the outcomes of stroke. For this multi-center study, we recruited 60 patients with anterior cerebral circulation occlusion and onset of stroke that had exceeded 4.5 h but lasted less than 48 h. These patients, after random division into two groups, received either standard management alone (controls) or standard management plus vinpocetine (30 mg per day intravenously for 14 consecutive days, Gedeon Richter Plc., Hungary). Vinpocetine treatment did not change the lymphocyte count; however, nuclear factor kappa-light-chain-enhancer of activated B cell activation was inhibited as seen not only by the increased transcription of IκBα mRNA but also by the impeded phosphorylation and degradation of IκBα and subsequent induction of pro-inflammatory mediators. These effects led to significantly reduced secondary lesion enlargement and an attenuated inflammation reaction. Compared to controls, patients treated with vinpocetine had a better recovery of neurological function and improved clinical outcomes during the acute phase and at 3-month follow-up. These findings identify vinpocetine as an inflammation modulator that could improve clinical outcomes after acute ischemic stroke. This study also indicated the important role of immunity and inflammation in the pathogenesis of acute ischemic stroke and the significance of immunomodulatory treatment.
CLINICAL TRIAL REGISTRATION INFORMATION: www.clinicaltrials.gov . Identifier: NCT02878772
Additional file 2: of Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models
Lymphocytes infiltration at day 14 after brain ischemia in ET-1 model. (A) ET-1 model induction. ET-1 and L-NAME were dissolved in sterile saline, and were delivered into the cortex by stereotaxic injection (AP +1.0, ML +1.0, DV -1.0, ET-1 at 1 μg and L-NAME at 2.7 μg). The ipsilateral common carotid artery were permanently occluded just prior to the ET-1 injection. (B) Lymphocyte infiltration at late stage of brain ischemia in mice subjected to ET-1 model. Dot plots of flow cytometry assay show CD4+ T, CD8+ T, NK, and B cells in single cell suspension from brains of sham (PBS injection) or ET-1/L-NAME injected mice at 14 days after procedures. (C) Bar graphs summarize the cumulative data for quantifying CD4+ T, CD8+ T, NK, and B cell counts from brains of ET-1 model at 14 days after stroke. n = 8 mice per group. Error bars represent s.e.m.; *P < 0.05; **P < 0.01, sham vs. ET-1 model by two-tailed unpaired Student’s t test. (DOCX 298 kb