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Glial activation analysis in the neuroimmunoendocrine alterations in septic rats and the simvastatin neuroprotector effect in survivals

Abstract

Sepsis, a systemic inflammation triggered by an infectious agent, produces an inflammatory state in the central nervous system (CNS) that leads to autonomic, endocrine and cognitive-behavioral dysfunctions observed in clinical and experimental studies. Previous findings from this laboratory suggest that oxidative stress, microglial activation, synaptic dysfunction and eventually apoptosis of neurons due to neuroinflammation and with neurodegenerative characteristics are responsible for these dysfunctions during and after sepsis. Thus, we suggest that sustained glial activation during sepsis would cause neuroimmunoendocrine changes and long-term neurological sequelae, leading to the establishment of neurodegenerative processes such as those occurring in the sporadic form of Alzheimer's disease. In this context, numerous drugs and therapies have been proposed to try to contain the effects of sepsis. For example, several clinical studies involving statins and sepsis are still very controversial about the benefits of this drug, leaving many gaps to be filled in order to reach a consensus on its use as a therapeutic strategy. Recently we have found that simvastatin improved the cognitive-behavioral aspects of rats survival sepsis. However, if the sepsis improvement is related to an effect of the drug in neurodegeneration and/or modulation of glial activation is unknown. Recently, we have found that simvastatin treatment improved the cognitive-behavioral aspects of rats surviving sepsis. Therefore, the objective of this study will be to evaluate the participation of glial activation in the neuroimmunoendocrine changes due to sepsis and the possible neuroprotective effect of simvastatin in surviving animals. (AU)

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VEICULO: TITULO (DATA)

Scientific publications (4)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DA COSTA, LUIS HENRIQUE ANGENENDT; SANTOS-JUNIOR, NILTON NASCIMENTO; CATALAO, CARLOS HENRIQUE ROCHA; ROCHA, MARIA JOSE ALVES. Microglial Activation Modulates Neuroendocrine Secretion During Experimental Sepsis. Molecular Neurobiology, v. 58, n. 5, . (18/02854-0, 16/07803-0)
VULCZAK, ANDERSON; ROCHA CATALAO, CARLOS HENRIQUE; PEDRO DE FREITAS, LUIZ ALEXANDRE; ALVES ROCHA, MARIA JOSE. HSP-Target of Therapeutic Agents in Sepsis Treatment. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v. 20, n. 17, . (18/02854-0)
CATALAO, CARLOS HENRIQUE ROCHA; SANTOS-JUNIOR, NILTON NASCIMENTO; DA COSTA, LUIS HENRIQUE ANGENENDT; SOUZA, ANDERSON OLIVEIRA; CARNIO, EVELIN CAPELLARI; SEBOLLELA, ADRIANO; ALBERICI, LUCIANE CARLA; ROCHA, MARIA JOSE ALVES. Simvastatin Prevents Long-Term Cognitive Deficits in Sepsis Survivor Rats by Reducing Neuroinflammation and Neurodegeneration. NEUROTOXICITY RESEARCH, v. 38, n. 4, p. 16-pg., . (18/10089-2, 17/12462-0, 18/02854-0)

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