[Irbesartan reduces inflammatory response of central nervous system in a rat model of fluid percussion brain injury].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Office of Clinical Administration, Fourth Military Medical University, Xi'an 710032, China. *Corresponding author, E-mail:

Published: July 2016

Objective To investigate the neuroprotective effect of the angiotensin II receptor 1 (AT1) antagonist irbesartan on rat models with lateral fluid percussion brain injury (FPBI). Methods FPBI models were prepared using a modified fluid percussion injury method. Before and after modeling, irbesartan was given to the rats. The regional cerebral blood flow (rCBF) was monitored by laser Doppler flowmetry. Neurologic status was evaluated before and 1, 3, 5, 7 days after FPBI surgery. Brains were removed for immunohistochemical evaluation of active microglias and macrophages. Results Compared to sham group, the rCBF and neurologic score of FPBI rats decreased significantly, while microglia and macrophage activation were confirmed. Treatment with irbesartan before FPBI surgery increased rCBF and improved neurological functions. In the peri-infarct cortex, irbesartan treatment attenuated the invasion of activated microglias and macrophages on day 7 after FPBI surgery. Conclusion Irbesartan can play a neuroprotective role through inhibiting microglia and macrophage activation in FPBI rats.

Download full-text PDF

Source

Publication Analysis

Top Keywords

fluid percussion
12
fpbi surgery
12
percussion brain
8
microglias macrophages
8
fpbi rats
8
microglia macrophage
8
macrophage activation
8
fpbi
7
irbesartan
5
[irbesartan reduces
4

Similar Publications

Traumatic brain injury (TBI) is one of the primary causes of mortality and disability, with arterial blood pressure being an important factor in the clinical management of TBI. Spontaneously hypertensive rats (SHRs), widely used as a model of essential hypertension and vascular dementia, demonstrate dysfunction of the hypothalamic-pituitary-adrenal axis, which may contribute to glucocorticoid-mediated hippocampal damage. The aim of this study was to assess acute post-TBI seizures, delayed mortality, and hippocampal pathology in SHRs and normotensive Sprague Dawley rats (SDRs).

View Article and Find Full Text PDF

: Traumatic brain injury (TBI) occurs after a sudden mechanical force to the skull and represents a significant public health problem. Initial brain trauma triggers secondary pathophysiological processes that induce structural and functional impairment of the central nervous system, even in the regions distant to the lesion site. Later in life, these changes can be manifested as neurodegenerative sequalae that commonly involve proteinopathies, such as transactive DNA-binding protein 43 (TDP-43).

View Article and Find Full Text PDF

Traumatic brain injury (TBI) is one of the major causes of severe neurological disorders and long-term dysfunction in the nervous system. Besides inducing neurodegeneration, TBI alters stem cell activity and neurogenesis within primary neurogenic niches. However, the fate of dividing cells in other brain regions remains unclear despite offering potential targets for therapeutic intervention.

View Article and Find Full Text PDF

Effects of a Serotonin Receptor Peptide on Behavioral Pattern Separation in Sham- vs. Mild Traumatic Brain Injured Rats.

Endocrinol Diabetes Metab J

June 2024

Medical & Research Services, Veterans Affairs New Jersey Healthcare System, East Orange, New Jersey, USA.

Aims: Behavioral pattern separation is a hippocampal-dependent component of episodic memory and a sensitive marker of early cognitive decline. Here we tested whether mild traumatic injury causes loss of pattern separation in the rat and for its prevention by a novel neuroprotective peptide fragment of the human serotonin 2A receptor (SN..

View Article and Find Full Text PDF

Repetitive cortical spreading depolarizations are prolonged early after experimental traumatic brain injury.

Exp Neurol

December 2024

Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45267, USA; Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, OH 45267, USA. Electronic address:

Cortical spreading depolarizations (CSDs) are the most common electrophysiological dysfunction following a traumatic brain injury (TBI), and clustered CSDs (≥3 CSDs in 2 h) are associated with poor outcomes 6 months after TBI. While many experimental studies have investigated a single CSD after injury, no known studies have investigated how time after injury affects the characteristics and impact of a CSD cluster. This study sought to determine the characteristics of a cluster of repetitive CSDs when induced at three different time points after moderate experimental TBI.

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!