2007
DOI: 10.1080/10790268.2007.11753925
|View full text |Cite
|
Sign up to set email alerts
|

Glutamine Concentration and Immune Response of Spinal Cord-Injured Rats

Abstract: Background/Objectives: Glutamine plays a key role in immune response. Spinal cord injury (SCI) leads to severe loss of muscle mass and to a high incidence of infections. This study investigated the acute effect of SCI (2 and 5 days) on the plasma glutamine and skeletal muscle concentrations and immune responses in rats. Methods: A total of 29 adult male Wistar rats were divided as follows: control (C; n ¼ 5), sham-operated (S2; n ¼ 5) and spinal cord-transected (T2; n ¼ 7). They were killed on day 2 after surg… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

1
16
0

Year Published

2010
2010
2022
2022

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 21 publications
(17 citation statements)
references
References 53 publications
1
16
0
Order By: Relevance
“…Spinal cord injury (SCI) leads to a complex series of cellular and molecular events including axotomy, demyelination of surviving axons, nucleotides release, free‐radical production, and release of excitatory amino acids (Franke et al, 2006; Tanhoffer et al, 2007). These events are followed by neural tissue loss due to necrosis, apoptosis, macrophage infiltration, and inflammation (Dijkstra et al, 2001; Hulsebosch, 2002; Iannotti et al, 2006; Popovich et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…Spinal cord injury (SCI) leads to a complex series of cellular and molecular events including axotomy, demyelination of surviving axons, nucleotides release, free‐radical production, and release of excitatory amino acids (Franke et al, 2006; Tanhoffer et al, 2007). These events are followed by neural tissue loss due to necrosis, apoptosis, macrophage infiltration, and inflammation (Dijkstra et al, 2001; Hulsebosch, 2002; Iannotti et al, 2006; Popovich et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…As summarized from some previous SCI research (Dumont et al, 2001;Ramer et al, 2005;Liu et al, 2006;Tanhoffer et al, 2007;Fehlings and Nguyen, 2010;Varnum and Ikezu, 2012;Zhang et al, 2012), secondary damage/injury after SCI has the following aspects: (1) timing: secondary damage mechanisms initiate within minutes after injury and last for weeks or months; (2) location: secondary damage is not only restricted to the area of the vertebral fracture, but also extends to adjacent segments and even influences the whole body; (3) mechanisms of damage: secondary injury following spinal cord trauma is multifactorial (McCormick, 1998;Ramer et al, 2005) (Table 1); (4) morphology: secondary damage after SCI is characterized by hematoma, edema, glial/axon scarring, and central cavitation; (5) cytokine secretion: pro-inflammatory cytokines and chemokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-6, IL-23, leukemia inhibitory factors (LIF) and inducible nitric oxide synthase (iNOS); and anti-inflammatory cytokines such as IL-10, IL-4, IL-13, and transforming growth factor β (TGF-β).…”
Section: Secondary Damage Following Scimentioning
confidence: 98%
“…Within the first minutes to hours after injury, a secondary cascade is initiated, which can last for weeks or months and whose damaging effects are comparative to, if not greater than, that of the initial insult (Tanhoffer et al, 2007;Oyinbo, 2011). Consequences of secondary injury include progressive axon demyelination (Totoiu and Keirstead, 2005), neuronal cell death (Beattie et al, 2002;Anwar et al, 2016), microglia activation and inflammation (Qiao et al, 2010(Qiao et al, , 2015, glial scar formation (Shibuya et al, 2009), and mitochondrial dysfunction, all of which contribute to the progressive pathology.…”
Section: Introductionmentioning
confidence: 99%