Vitamin C alleviates LPS-induced cognitive impairment in mice by suppressing neuroinflammation and oxidative stress
Autor: | Qiang Fu, Li-Ming Zhang, Jiangbei Cao, Zhipeng Xu, Wei Wang, Yun-Feng Li, Weidong Mi, Yang Li, Xiao-Ying Zhang, Xiu-Lin Huo, Weixing Zhao |
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Rok vydání: | 2018 |
Předmět: |
Lipopolysaccharides
Male 0301 basic medicine medicine.medical_specialty medicine.drug_class Immunology Anti-Inflammatory Agents Morris water navigation task Ascorbic Acid medicine.disease_cause p38 Mitogen-Activated Protein Kinases Immunostimulant Superoxide dismutase Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Malondialdehyde Internal medicine Animals Humans Immunology and Allergy Medicine Memory impairment Cognitive Dysfunction Maze Learning Neuroinflammation Pharmacology Memory Disorders biology business.industry Mice Inbred C57BL Disease Models Animal Oxidative Stress 030104 developmental biology Endocrinology chemistry biology.protein Cytokines Tumor necrosis factor alpha Neurogenic Inflammation business 030217 neurology & neurosurgery Oxidative stress Signal Transduction |
Zdroj: | International Immunopharmacology. 65:438-447 |
ISSN: | 1567-5769 |
Popis: | Neuroinflammation is believed to be one of the primary causes of cognitive impairment. Previous studies showed that the antioxidant vitamin C (Vit C) performs many beneficial functions such as immunostimulant and anti-inflammatory actions, but its role in inflammatory cognitive impairment is unclear. In the current study, we investigated the effect and possible mechanism of action of Vit C in lipopolysaccharide (LPS)-induced cognitive impairment. Intracerebroventricular LPS-induced memory impairment was used as the model for neuroinflammatory cognitive dysfunction. Vit C was administered by intracerebroventricular microinjection 30 min prior to LPS exposure. It was found that Vit C significantly protected animals from LPS-induced memory impairment as evidenced by improved performance in the Morris water maze and novel object recognition tests without changes in spontaneous locomotor activity. Vit C pretreatment inhibited the activation of microglia and the production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Furthermore, Vit C pretreatment markedly decreased the malondialdehyde (MDA) level, increased superoxide dismutase (SOD) activity, and modulated the Bax/Bcl-2 ratio and p-p38 MAPK activation in the hippocampus of LPS-treated mice. Together, these results suggest that vitamin C pretreatment could protect mice from LPS-induced cognitive impairment, possibly through the modulation of oxidative stress and inflammatory responses. |
Databáze: | OpenAIRE |
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