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The present study aimed to investigate the therapeutic effects of curcumin (CU) against brain edema in a rat model of hypoxia-hypercapnia (HH)-induced brain damage (HHBD). Male Sprague-Dawley rats were divided into five groups, including a control group and four treatment groups. The rats in the control group were raised under normal laboratory conditions and were injected with water, whereas the rats in the treatment groups were exposed to a low O/high CO environment simulating HH conditions, and were injected with water, CU, dimethyl sulfoxide (solvent control) or monosialoganglioside GM1. After 2 weeks, the morphological characteristics of the brain tissues were analyzed using optical and electron microscopy. In addition, aquaporin (AQP)-4 protein expression levels in brain tissue samples were analyzed using streptavidin-biotin complex immunohistochemistry and western blotting, and mRNA expression levels were detected using reverse transcription-quantitative polymerase chain reaction. Severe brain edema, tissue structure disruption and increased AQP4 expression levels were detected in the brain tissues of the HH rats. Conversely, the rats treated with CU or GM1 exhibited attenuated HHBD-induced brain edema and tissue structure disruption, and decreased mRNA and protein expression levels of AQP4. The results of the present study suggested that CU treatment was able to attenuate HHBD-induced brain edema by downregulating the expression levels of AQP4 in a rat model. Therefore, CU may be considered a potential therapeutic drug for the treatment of patients with brain edema.
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http://dx.doi.org/10.3892/etm.2016.3022 | DOI Listing |
J Neurooncol
September 2025
Division of Neurosurgery, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, Tottori, Japan.
Purpose: This study aimed to evaluate the prognostic significance of microvessel density (MVD), assessed by CD34 immunohistochemistry (IHC), and its correlation with radiological features and bevacizumab (BEV) treatment efficacy in newly diagnosed glioblastoma.
Methods: We retrospectively analyzed 41 patients with newly diagnosed glioblastoma. MVD was quantified using CD34 IHC, and patients were stratified into low and high MVD groups according to the cutoff value determined by receiver operating characteristic curve analysis (sensitivity, 76.
Int J Emerg Med
September 2025
Family Medicine Department, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Background: Acute necrotizing encephalopathy is a rare but severe neurological disorder characterized by rapid onset of fever, altered mental status, seizures, and multifocal brain lesions, particularly involving the thalami and brainstem. Often triggered by viral infections, its pathogenesis involves a hyperinflammatory response, resulting in blood-brain barrier disruption and necrosis of neural tissue. While influenza and herpesviruses are common etiological agents, adenovirus is a less frequently reported cause.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Anesthesiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 XianXia Road, Shanghai 200336, China; Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 1111 XianXia Road, Shanghai 200336, China. El
Hypoxic-ischemic brain damage (HIBD) is a severe condition leading to extensive neuronal loss and functional impairments, representing a significant challenge in neonatal care. PFGA12, a peptide derived from fibrinogen alpha chain (FGA), which is notably downregulated in the umbilical cord blood of hypoxic-ischemic encephalopathy (HIE) infants. We demonstrate that PFGA12 significantly enhances cell viability and mitigates oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal cell death.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
September 2025
Department of Rehabilitation Medicine, Hebei Engineering University Affiliated Hospital, Handan, Hebei, China.
Blood-Brain Barrier (BBB) dysfunction acts as a key mediator of ischemic brain injury, contributing to brain edema, inflammatory cell infiltration, and neuronal damage. The integrity of the BBB is largely maintained by tight junction proteins, such as Claudin-5, and its disruption exacerbates neurological deficits. Neurokinin B (NKB), a neuropeptide that belongs to the tachykinin family, has been implicated in various physiological processes, including neuroinflammation and vascular function.
View Article and Find Full Text PDFFront Surg
August 2025
Department of Neurology, University Hospital and Faculty of Medicine and Dentistry, Palacký University, Olomouc, Czechia.
Introduction: Peri-lead edema (PLE) is a commonly observed but often asymptomatic complication of deep brain stimulation (DBS). While usually transient and benign, severe cases of PLE can result in neurological symptoms, impacting patient outcomes. This case series explores the clinical course, management, and outcomes of symptomatic PLE in a series of five patients undergoing DBS.
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