Objectives: Curcumin is a molecule found in turmeric root that possesses anti-inflammatory and antioxidant properties and has been widely used to treat neurodegenerative diseases. We investigated whether curcumin stimulates the neurorepair process and improves locomotor function in a rat model of spinal cord ischemia-reperfusion injury.
Methods: Thirty-two Wistar albino rats (190-220 g) were randomly allocated into 4 groups of 8 rats each: 1 sham-operated group and 3 ischemia-reperfusion injury groups that received intraperitoneal injections of saline vehicle, methylprednisolone (MP, 30 mg/kg following induction of ischemia-reperfusion [IR] injury), or curcumin (200 mg/kg for 7 days before induction of IR injury). Spinal cord IR injury was induced by occlusion of the abdominal aorta for 30 minutes. After 24 hours of reperfusion, locomotor function was assessed using the Basso, Beattie, and Bresnahan scale. All animals were sacrificed. Spinal cord tissues were harvested to evaluate histopathological and ultrastructural alterations and to analyze levels of malondialdehyde, tumor necrosis factor-alpha, interleukin-1 beta, nitric oxide, and caspase-3, as well as enzyme activities of superoxide dismutase and glutathione peroxidase.
Results: Intraperitoneal administration of curcumin significantly reduced inflammatory cytokine expression, attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in comparison to treatment with MP or saline. Histopathological and ultrastructural abnormalities were significantly reduced in curcumin-treated rats compared to the MP- and saline-treated groups. Furthermore, curcumin significantly improved locomotor function.
Conclusions: Curcumin treatment preserves neuronal viability against inflammation, oxidative stress, and apoptosis associated with ischemia-reperfusion injury.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.01.008 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Multiple sclerosis and sickle cell anemia: when two worlds collide.
Neurol Sci
January 2025
Hematology Unit, Careggi University Hospital, Florence, Italy.
Background: The coexistence of sickle cell anemia and multiple sclerosis in a single patient presents a rare and challenging clinical scenario, possibly favoured by the interplay between chronic inflammatory states and autoimmune processes.
Methos/results: We present the case of a 36-year-old woman with sickle cell anemia who developed progressive neurological symptoms leading to frequent falls and paraparesis; magnetic resonance imaging showed many periventricular, infratentorial, and both cervical and dorsal spinal cord lesions, leading to a diagnosis of multiple sclerosis. After a multidisciplinary approach the patient was successfully started on ofatumumab.
A Rare Case of Spinal Hypertrophic Pachymeningitis That Caused Tetraplegia After Myelography.
Cureus
December 2024
Department of Orthopaedics, Tokyo Metropolitan Bokutoh Hospital, Tokyo, JPN.
Hypertrophic pachymeningitis (HP) is a rare inflammatory disease that causes the thickening of the dura mater. Its etiology is mainly classified as idiopathic or secondary, and autoimmune disease is one of the main causes of secondary HP. Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis and IgG4-related disease are common among autoimmune diseases.
View Article and Find Full Text PDFSpinal astrocyte-derived interleukin-17A promotes pain hypersensitivity in bone cancer mice.
Acta Pharm Sin B
December 2024
Department of Translational Neuroscience, Jing'an District Centre Hospital of Shanghai, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai 200032, China.
Spinal microglia and astrocytes are both involved in neuropathic and inflammatory pain, which may display sexual dimorphism. Here, we demonstrate that the sustained activation of spinal astrocytes and astrocyte-derived interleukin (IL)-17A promotes the progression of mouse bone cancer pain without sex differences. Chemogenetic or pharmacological inhibition of spinal astrocytes effectively ameliorates bone cancer-induced pain-like behaviors.
View Article and Find Full Text PDFAmantadine modulates novel macrophage phenotypes to enhance neural repair following spinal cord injury.
J Transl Med
January 2025
Department of Neurosurgery, The Second Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, China.
Background: Spinal cord injury (SCI) triggers a complex inflammatory response that impedes neural repair and functional recovery. The modulation of macrophage phenotypes is thus considered a promising therapeutic strategy to mitigate inflammation and promote regeneration.
Methods: We employed microarray and single-cell RNA sequencing (scRNA-seq) to investigate gene expression changes and immune cell dynamics in mice following crush injury at 3 and 7 days post-injury (dpi).
Clinical spectrum of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia in individuals of Korean ancestry.
Sci Rep
January 2025
Department of Neurology, Neuroscience Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 06351, Korea.
Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a rare white matter disease characterized by axonal and glial injury. Although its clinical characteristics have been described in case reports, the prevalence of CSF1R mutations in clinically suspected ALSP cases remains unclear. Herein, we analysed the frequency of CSF1R mutations in patients with probable or possible ALSP and describe the genetic, clinical, radiological, and pathological findings of ALSP cases in individuals of Korean ancestry.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!