Glutamine‐induced heat shock protein protects against renal ischaemia‐reperfusion injury in rats

Zou, Zui; Li, Yingke; Yuan, Haitao; Xue-yin, Shi

doi:10.1111/j.1440-1797.2009.01108.x

Cited by 19 publications

(19 citation statements)

References 20 publications

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“…Our data on apoptosis are in accordance with the study of Zhang et al (2009) showing that glutamine pretreatment in rats was effective in alleviating the injury and apoptosis after kidney warm ischemic process. The animal model and administration route described by Zhang et al (2009) were different from ours, because intravenous injection of glutamine 1 h before renal warm I/R injury was used.…”

Section: Discussionsupporting

confidence: 95%

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Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Esposito

Mondello

Paola

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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The aim of this study was to investigate the effects of glutamine in an in vivo rat model of renal ischemia/reperfusion (I/R) injury. Male Wistar rats underwent bilateral renal pedicle clamping for 45 min followed by reperfusion for 6 h. Glutamine (1.5 mg/kg) was administered intraperitoneally (i.p.) 15 min prior to reperfusion. Plasma concentrations of urea, creatinine, γ-glutamyl transferase (γ-GT), and aspartate aminotransferase (AST) were measured for the assessment of renal function and reperfusion injury. Markers of oxidative stress, expression of the pro-inflammatory mediators inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), AT-1 expression, and changes in the oxidative stress-sensitive nuclear factor kappa B (NF-κB) signaling pathway were measured to investigate whether glutamine can reduce the renal dysfunction. Kidney myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels were measured for assessment of polymorphonuclear (PMN) cell infiltration and lipid peroxidation, respectively. Renal sections were used for histologic grading of renal injury and for immunohistochemical localization of nitrotyrosine and poly(ADP-ribose) synthetase (PARS). In vivo, glutamine significantly reduced the increase in urea, creatinine, γ-GT, AST, produced by renal ischemia/reperfusion (I/R), suggesting an improvement in both renal function and injury. Glutamine significantly reduced iNOS and NF-κB, kidney MPO activity and MDA levels, indicating a reduction in PMN infiltration and lipid peroxidation, respectively. Glutamine reduced the histological evidence of renal damage associated with I/R and caused a substantial reduction in the staining for nitrotyrosine and PARS, suggesting reduced nitrosative and oxidative stress. Moreover, glutamine attenuated the reduction of COX-2 expression and prevented the increased AT-1 expression after I/R. Our results suggest that glutamine reduces the renal dysfunction and injury associated with I/R of the kidney.

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Section: Discussionsupporting

confidence: 95%

“…The animal model and administration route described by Zhang et al (2009) were different from ours, because intravenous injection of glutamine 1 h before renal warm I/R injury was used. Moreover, reperfusion periods chosen were 6 and 24 h, because HSP expression pattern was described.…”

Section: Discussionmentioning

confidence: 99%

Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Esposito

Mondello

Paola

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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“…In fact, glutamine attenuates endotoxin-induced lung metabolic dysfunction [221] and reduces lung injury after sepsis, thus improving survival, by enhancing HSP70 expression [222,223]. Moreover, glutamine protects against renal ischemia-reperfusion injury [224]. This is because glutamine protects against cellular injury by increasing HSF1 function [225].…”

Section: Glutamine Metabolism and Its Importance For The Heat Shock Rmentioning

confidence: 99%

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

Leite

Cruzat

Krause

et al. 2016

Nutrire

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Aging is an intricate process modulated by different molecular and cellular events, such as genome instability, epigenetic and transcriptional changes, molecular damage, cell death and senescence, inflammation, and metabolic dysfunction. Particularly, protein quality control (chaperone systems) tends to be negatively affected by aging, thus leading to cellular senescence in metabolic tissues and, as a consequence, to the increasing dissemination of inflammation throughout the body. The heat shock (HS) response and its associated expression of the 70 kDa family of heat shock proteins (HSP70), which are anti-inflammatory molecular chaperones, are found to be markedly decreased during muscle inactivity and aging, while evidence supports the loss of HSP70 as a key mechanism which may drive muscle atrophy, contractile dysfunction, and reduced regenerative capacity. In addition, abnormal stress response is linked with higher incidence of neurodegenerative diseases as well as low-grade inflammatory diseases that are associated with physical inactivity and obesity. Therefore, strategies to increase or, at least, to maintain the levels of HSP70, and its accompanying HS response to stress, are key to reduce biological cell dysfunctions that occur in aging. In this sense, physical exercise is of note as it is the most powerful inducer of the HS response, comparable only to heat stress and fever-like conditions. On the other hand, the amino acid L-glutamine, whose production within the skeletal muscle and liberation into the blood stream is dependent on muscle activity, is a potentializer of HSP70 expression and HS response, particularly via its entering in hexosamine biosynthetic pathway (HBP). Herein, we discuss the collaborative role of glutamine (and its donors/precursors) and physical exercise (mostly responsible for glutamine release into the circulation) as potential tools to increase HSP70 expression and the HS response in the elderly.

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“…& Wischmeyer, P.E., 2008) in a process that is mediated, at least partially, by the increase in the flux through the hexosamine biosynthetic pathway (Hamiel et al, 2009). Also, it has been shown that a single dose of L-glutamine relieve renal ischaemia-reperfusion injury in rats in 24 h by a mechanism associated with enhanced HSP70 expression (Zhang et al, 2009). …”

Section: Intracellular Hsp70mentioning

confidence: 99%

“…Conversely, in LPS-endotoxemic rats, a single dose of L-glutamine, which is known to induce anti-inflammation via HSP70 expression (Wischmeyer et al, 2003;Singleton, K.D. & Wischmeyer, P.E., 2008;Hamiel et al, 2009;Zhang et al, 2009) has been shown to attenuate the release of TNF and IL-1 and to be associated with a significant www.intechopen.com decrease in mortality due to the attenuation of pro-inflammatory type 1 cytokines (Wischmeyer et al, 2001), whereas L-arginine-enriched diet limits plasma and muscle L-glutamine depletion in head-injured rats (Moinard et al, 2006). Remarkably, however, predominately Th1 (but not Th2) cell responses require the presence of optimal concentrations of L-glutamine (Chang et al, 1999).…”

Section: Participation Of L-arginine/l-glutamine Coupling In Diabetesmentioning

confidence: 99%

A Novel L-Arginine/L-Glutamine Coupling Hypothesis: Implications for Type 1 Diabetes

Bittencourt¹,

Newsholme²

2011

Type 1 Diabetes - Complications, Pathogenesis, and Alternative Treatments

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Glutamine‐induced heat shock protein protects against renal ischaemia‐reperfusion injury in rats

Cited by 19 publications

References 20 publications

Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Glutamine contributes to ameliorate inflammation after renal ischemia/reperfusion injury in rats

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

A Novel L-Arginine/L-Glutamine Coupling Hypothesis: Implications for Type 1 Diabetes

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