Objective: To explore the relationship between miR-7-5p and brain edema after intracerebral hemorrhage and the role of butylphthalide (NBP) in brain edema after intracerebral hemorrhage.Method: Routine blood testing, C-reactive protein results, and computed tomography data were collected 1, 7, and 14 days after intracerebral hemorrhage in six patients. Levels of MMP-9, ZO-1, occludin, IL-6, TNF-α, and miR-7-5p were detected in each patient's serum. Sixty male Sprague–Dawley rats were randomly divided into sham operation, intracerebral hemorrhage, and NBP treatment groups. Dry–wet weight was used to assess brain edema, and Evans blue staining was used to assess the permeability of the blood–brain barrier. Expression levels of IL-6, TNF-α, ZO-1 and occludin, PI3K, AKT, p-AKT, AQP4, and miR-7-5p were analyzed in the rat brains.Result: The blood neutrophil–lymphocyte ratio (NLR) on day 1 was associated with the area of brain edema on day 7. The expression of miR-7-5p decreased after intracerebral hemorrhage, and as a result, the inhibition of the PI3K/AKT pathway was weakened. The decreased inhibition of the PI3K/AKT pathway resulted in an increase in AQP4 expression, which further aggravated brain edema. NBP can upregulate the expression of miR-7-5p, affecting these pathways to reduce brain edema.Conclusion: After intracerebral hemorrhage, miR-7-5p expression in brain tissue is reduced, which may increase the expression of AQP4 by activating the PI3K/AKT pathway. NBP can inhibit this process and reduce brain edema.
Guillain-Barré syndrome (GBS) is mainly associated with preceding exposure to an infectious agent, although the precise pathogenic mechanisms and causes remain unknown. Increasing evidence indicates an association between trauma-related factors and GBS. Here, we performed a systematic review, summarized the current scientific literature related to the onset of GBS associated with trauma, and explored the possible pathogenesis. A literature search of various electronic databases was performed up to May 2020 to identify studies reporting diverse trauma-related triggers of GBS. Data were extracted, summarized descriptively, and evaluated with respect to possible mechanisms. In total, 100 publications, including 136 cases and 6 case series involving GBS triggered by injury, surgery, intracranial hemorrhage, and heatstroke, met our eligibility criteria. The median age of the patients was 53 [interquartile range (IQR) 45-63] years, and 72.1% of the patients were male. The median number of days between the trigger to onset of GBS symptoms was 9 (IQR 6.5-13). Overall, 121 patients (89.0%) developed post-injury/surgical GBS, whereas 13 (9.6%) and 2 (1.5%) patients had preexisting spontaneous intracranial hemorrhage and heatstroke, respectively. The main locations of injury or surgeries preceding GBS were the spine and brain. Based on available evidence, we highlight possible mechanisms of GBS induced by these triggers. Moreover, we propose the concept of "trauma-related GBS" as a new research direction, which may help uncover more pathogenic mechanisms than previously considered for typical GBS triggered by infection or vaccination.
Inflammation and immunity play an essential role in disease pathogenesis. 3-N-Butylphthalide (NBP), a group of compounds extracted from seeds of Apium graveolens (Chinese celery), has been demonstrated as an efficient and effective therapy for ischemic stroke. The amount of research on NBP protective effect is increasing at pace, such as microcircular reconstruction, alleviating inflammation, ameliorating brain edema and blood-brain barrier (BBB) damage, mitochondrial function protection, antiplatelet aggregation, antithrombosis, decreasing oxidative damage, and reducing neural cell apoptosis. There has been increasing research emphasizing the association between NBP and immunity and inflammation in the past few years. Hence, it is aimed at reviewing the related literature and summarizing the underlying anti-inflammatory and immunoregulatory function of NBP in various disorders.
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