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}
}
Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress
TLDR
It is shown that troxerutin inhibits cyclin-dependent kinase 1 expression, enhances type 1 protein phosphatase α dephosphorylation, and abolished MEK/ERK1/2/C/EBP β activation, which subsequently reverses the memory impairment observed in the DA-treated mice.
Ursolic acid improves domoic acid-induced cognitive deficits in mice.
Low molecular weight heparin prevents lipopolysaccharide induced-hippocampus-dependent cognitive impairments in mice.
TLDR
Low-molecular-weight heparin (LMWH) treatment protects against sepsis-induced cognitive impairments by attenuating hippocampal microglial activation, cytokine and oxidative stress production, disruption of blood-brain barrier, and the loss of synaptic plasticity related proteins.
Ursolic Acid Ameliorates Inflammation in Cerebral Ischemia and Reperfusion Injury Possibly via High Mobility Group Box 1/Toll-Like Receptor 4/NFκB Pathway
TLDR
Novel evidence is provided that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.
Ursolic acid isolated from the seed of Cornus officinalis ameliorates colitis in mice by inhibiting the binding of lipopolysaccharide to Toll-like receptor 4 on macrophages.
TLDR
Findings suggest that ursolic acid may ameliorate colitis by regulating NF-κB and MAPK signaling pathways via the inhibition of LPS binding to TLR4 on immune cells.
Neuroprotection of Rotenone induced Parkinsonism by Ursolic acid in PD mouse model.
TLDR
The results obtained have suggested that UA significantly reduced the overexpression of α-Synuclein and regulated the phosphorylation of survival-related kinases (Akt and ERK) apart from alleviating the behavioral abnormalities and protecting the dopaminergic neurons from oxidative stress and neuroinflammation.
Ursolic acid reduces the metalloprotease/anti-metalloprotease imbalance in cerebral ischemia and reperfusion injury
TLDR
Ursolic acid can act as a PPARγ agonist to improve the metalloprotease/anti-metalloproteinase balance, possibly by inhibiting the activation of the MAPK signaling pathway, thereby attenuating cerebral ischemia and reperfusion injury.
Ursolic acid ameliorates autoimmune arthritis via suppression of Th17 and B cell differentiation
TLDR
Ursolic acid treatment significantly ameliorates CIA in mice via suppression of Th17 and differentiation, and may be useful for the treatment of autoimmune arthritis and other Th17-related diseases.
...
1
2
3
4
5
...

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.
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.
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.
...
1
2
3
4
5
...