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
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
Externí odkaz: