Ursolic acid attenuates lipopolysaccharide-induced cognitive deficits in mouse brain through suppressing p38/NF-κB mediated inflammatory pathways

@article{Wang2011UrsolicAA,
  title={Ursolic acid attenuates lipopolysaccharide-induced cognitive deficits in mouse brain through suppressing p38/NF-$\kappa$B mediated inflammatory pathways},
  author={Yong-Jian Wang and Jun Lu and Dong-Mei Wu and Zi-hui Zheng and Yuanlin Zheng and Xiao-hui Wang and Jie Ruan and Xiao Sun and Qun Shan and Zi‐feng Zhang},
  journal={Neurobiology of Learning and Memory},
  year={2011},
  volume={96},
  pages={156-165}
}
Evidence indicates that systemic administration of lipopolysaccharide (LPS) induces brain inflammation, ultimately resulting in cognitive deficits. Ursolic acid (UA), a plant-derived pentacyclic triterpenoid, is well known to possess multiple biological functions, including antioxidant, anti-tumor and anti-inflammatory activities. In the present study, we assessed the protective effect of UA against the LPS-induced cognitive deficits in mice. We found that UA significantly improved cognitive… 
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References

SHOWING 1-10 OF 42 REFERENCES
Ursolic acid attenuates D-galactose-induced inflammatory response in mouse prefrontal cortex through inhibiting AGEs/RAGE/NF-κB pathway activation.
TLDR
Ursolic acid administration significantly improved behavioral performance of D-gal-treated mice in step-through test and Morris water maze task and significantly decreased AGEs induced the expression of receptor for advanced glycation end products and inhibited NF-κB p65 nuclear translocation in the prefrontal cortex of D -gal- treated mice.
Purple sweet potato color suppresses lipopolysaccharide-induced acute inflammatory response in mouse brain
TLDR
Data suggest that PSPC may be useful for mitigating inflammatory brain diseases by the inhibition of proinflammatory molecule production, at least in part, through blocking ERK, JNK and NF-kappaB signaling.
Aggregated Ursolic Acid, a Natural Triterpenoid, Induces IL-1β Release from Murine Peritoneal Macrophages: Role of CD361
TLDR
Results indicate that aggregated UA is recognized, in part, by CD36 on macrophages for generating ROS, thereby activating p38 MAPK, ERK1/2, and caspase-1, as well as releasing IL-1β protein via the ATP-binding cassette transporter.
Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion
TLDR
It is indicated that stress, via GC secretion, can increase LPS-induced NF-κB activation in the frontal cortex and hippocampus, agreeing with a growing literature demonstrating proinflammatory effects of GCs.
Ursolic acid ameliorates cognition deficits and attenuates oxidative damage in the brain of senescent mice induced by D-galactose.
TLDR
The results indicated that the neuroprotective effect of UA against D-gal induced neurotoxicity might be caused, at least in part, by the increase in the activity of antioxidant enzymes with a reduction in lipid peroxidation.
Vitamin E suppression of microglial activation is neuroprotective
TLDR
Results suggest that, in addition to the beneficial effects of providing direct antioxidant protection to neurons reported by others, vitamin E may provide neuroprotection in vivo through suppression of signaling events necessary for microglial activation.
Central and Systemic Endotoxin Challenges Exacerbate the Local Inflammatory Response and Increase Neuronal Death during Chronic Neurodegeneration
TLDR
Both central and peripheral inflammation can exacerbate local brain inflammation and neuronal death, and the finding that a single acute systemic inflammatory event can induce neuronal death in the CNS has implications for therapy in neurodegenerative diseases.
Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein
TLDR
New insights are provided in mouse models of AD, revealing TNF-α and iNOS as central mediators of Aβ action and these pathways might be targeted for AD drug development.
Role of Microglial-Derived Tumor Necrosis Factor in Mediating CD14 Transcription and Nuclear Factor κ B Activity in the Brain during Endotoxemia
TLDR
The present data provide the evidence that microglial-derived TNF-α is responsible for the production of the LPS receptor CD14 during endotoxemia and may be of great importance in controlling the inflammatory events that take place in the CNS during innate immune response as well as under pathological conditions.
Ursolic acid protects hippocampal neurons against kainate-induced excitotoxicity in rats
TLDR
The results suggest that multiple mechanisms including modulation of AMPA receptor, protection of mitochondria, decrease in free radical generation, and scavenging of free radicals might be involved in ursolic acid protection against kainate-induced cell toxicity.
...
1
2
3
4
5
...