Neuroinflammation is associated with a number of neurodegenerative diseases. It is known that lipopolysaccharide (LPS) treatment induces neuroinflammation and memory deterioration. Agmatine, the metabolite of arginine by arginine decarboxylase, is suggested to be a neuroprotective agent. The aim of this study was to explore if agmatine can prevent LPS-induced spatial memory impairment and hippocampal apoptosis. Adult male Wistar rats (200-250 g) were trained in water maze for 4 days (3 days in hidden platform and the last day in visible platform task). Saline, LPS (250 microg/kg/ip) or (and) agmatine (5 or 10 mg/kg) were administered 4h before every training session. LPS treatment impaired water maze place learning while agmatine co-administration prevented it. Also western blot studies revealed that LPS induces hippocampal caspase-3 activation while agmatine treatment prevented it.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ejphar.2010.02.029DOI Listing

Publication Analysis

Top Keywords

lps-induced spatial
8
spatial memory
8
memory impairment
8
impairment hippocampal
8
hippocampal apoptosis
8
lps treatment
8
water maze
8
agmatine
6
agmatine prevents
4
prevents lps-induced
4

Similar Publications

Infections of the nervous system, such as acute bacterial meningitis, pose serious health problems that require immediate intervention. In experimental animals, exposure to lipopolysaccharide (LPS) is used to induce meningitis. Aside from drug intervention to reduce inflammation in meningitis, aerobic exercise helps to maintain the regulatory mechanisms of brain homeostasis through anti-inflammatory mechanisms.

View Article and Find Full Text PDF

HDAC10 switches NLRP3 modification from acetylation to ubiquitination and attenuates acute inflammatory diseases.

Cell Commun Signal

December 2024

Department of Immunology, School of Basic Medical Sciences, Cheeloo college of Medicine, Shandong University, Jinan, 250012, China.

Background: The NOD-like receptor protein (NLRP)3 inflammasome is at the signaling hub center to instigate inflammation in response to pathogen infection or oxidative stress, and its tight control is pivotal for immune defense against infection while avoiding parallel intensive inflammatory tissue injury. Acetylation of NLRP3 is critical for the full activation of NLRP3 inflammasome, while the precise regulation of the acetylation and deacetylation circuit of NLRP3 protein remained to be fully understood.

Methods: The interaction between histone deacetylase 10 (HDAC10) and NLRP3 was detected by immunoprecipitation and western blot in the HDAC10 and NLRP3 overexpressing cells.

View Article and Find Full Text PDF

Brain inflammation and oxidative stress play critical roles in neuronal apoptosis and memory dysfunction in Alzheimer's disease. Crocin, a natural carotenoid in the stigma of saffron, possesses radical scavenging, anti-inflammatory, and anti-apoptotic properties. This study investigates the protective impact of crocin on neuronal apoptosis, oxidative stress, neuroinflammation, and memory deficits induced by lipopolysaccharide (LPS) in rats.

View Article and Find Full Text PDF

Astrocytes regulate brain functions through gliotransmitters like ATP/ADP and glutamate, but their release patterns and mechanisms remain controversial. Here, we visualized ATP/ADP and glutamate response following astrocyte activation and investigated their mechanisms in vivo. Employing cOpn5-mediated optogenetic stimulation, genetically encoded fluorescent sensors, and two-photon imaging, we observed ATP/ADP released as temporally prolonged and spatially extended flashes that later converted to adenosine.

View Article and Find Full Text PDF

New insights on targeting extracellular vesicle release by GW4869 to modulate lipopolysaccharide-induced neuroinflammation in mice model.

Nanomedicine (Lond)

December 2024

Department of Neurosurgery, Xi'an Central Hospital, Xi'an Jiaotong University. No. 161, West 5a Road, Xincheng District, Xi'an, 710003, P.R. China.

Article Synopsis
  • This study investigates how the release of extracellular vesicles (EVs) from glial cells affects microglia-astrocyte interactions and influences neurological outcomes.
  • Using a pharmacological agent (GW4869), researchers found that reducing EV release lowered inflammation and altered behavioral responses in mouse models induced by lipopolysaccharide (LPS).
  • The results suggest that manipulating EV dynamics may offer a new therapeutic strategy for treating neurological disorders by reducing neuroinflammation and improving cognitive functions and behavior.
View Article and Find Full Text PDF

Want 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!