Methylene Blue Protects Liver Oxidative Capacity after Gut Ischaemia–Reperfusion in the Rat

Collange, Olivier; Charles, Anne; Bouitbir, Jamal; Chenard, M.P.; Zoll, Joffrey; Diemunsch, Pierre; Thaveau, Fabien; Chakfé, Nabil; Piquard, François; Gény, Bernard

doi:10.1016/j.ejvs.2012.11.011

Cited by 23 publications

(29 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Liver damage related to lower limb ischemia-reperfusion was less demonstrated but, in view of the detoxification role of the liver, it might concentrate inflammatory cells triggered by lower limb IR and should be affected, as previously reported in the setting of gut IR [13]. …”

Section: Introductionmentioning

confidence: 73%

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Mansour

Charles

Kindo

et al. 2014

BioMed Research International

Self Cite

View full text Add to dashboard Cite

Remote organ impairments are frequent and increase patient morbidity and mortality after lower limb ischemia-reperfusion (IR). We challenged the hypothesis that lower limb IR might also impair lung, renal, and liver mitochondrial respiration. Two-hour tourniquet-induced ischemia was performed on both hindlimbs, followed by a two-hour reperfusion period in C57BL6 mice. Lungs, liver and kidneys maximal mitochondrial respiration (V max⁡), complexes II, III, and IV activity (V succ), and complex IV activity (V TMPD) were analyzed on isolated mitochondria. Lower limb IR decreased significantly lung V max⁡ (29.4 ± 3.3 versus 24 ± 3.7 μmol O2/min/g dry weight, resp.; P = 0.042) and tended to reduce V succ and V TMPD. IR did not modify liver but increased kidneys mitochondrial respiration (79.5 ± 19.9 versus 108.6 ± 21.4, P = 0.035, and 126 ± 13.4 versus 142.4 ± 10.4 μmol O2/min/g dry weight for V max⁡ and V succ, resp.). Kidneys mitochondrial coupling was increased after IR (6.5 ± 1.3 versus 8.8 ± 1.1, P = 0.008). There were no histological changes in liver and kidneys. Thus, lung mitochondrial dysfunction appears as a new early marker of hindlimb IR injuries in mice. Further studies will be useful to determine whether enhanced kidneys mitochondrial function allows postponing kidney impairment in lower limb IR setting.

show abstract

Section: Introductionmentioning

confidence: 73%

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Mansour

Charles

Kindo

et al. 2014

BioMed Research International

Self Cite

View full text Add to dashboard Cite

show abstract

“…Traumatic brain injury [13] is defined as an insult to the brain caused by an external physical force, leading to an alteration in brain functioning [14]. The Centers for Disease Control and Prevention estimates that at least 1.7 million cases of TBI occur in the United States annually [15], and is steadily on the rise.…”

Section: Introductionmentioning

confidence: 99%

Targeting mitochondrial dysfunction in CNS injury using Methylene Blue; still a magic bullet?

Vekaria

Watts

Lin

et al. 2017

Neurochemistry International

View full text Add to dashboard Cite

Complex, multi-factorial secondary injury cascades are initiated following traumatic brain injury, which makes this a difficult disease to treat. The secondary injury cascades following the primary mechanical tissue damage, are likely where effective therapeutic interventions may be targeted. One promising therapeutic target following brain injury are mitochondria. Mitochondria are complex organelles found within the cell, which act as powerhouses within all cells by supplying ATP. These organelles are also necessary for calcium cycling, redox signaling and play a major role in the initiation of cell death pathways. When mitochondria become dysfunctional, there is a tendency for the cell to loose cellular homeostasis and can lead to eventual cell death. Targeting of mitochondrial dysfunction in various diseases has proven a successful approach, lending support to mitochondria as a pivotal player in TBI cell death and loss of behavioral function. Within this mixed mini review/research article there will be a general discussion of mitochondrial bioenergetics, followed by a brief discussion of traumatic brain injury and how mitochondria play an integral role in the neuropathological sequelae following an injury. We will also give an overview of one relatively new TBI therapeutic approach, Methylene Blue, currently being studied to ameliorate mitochondrial dysfunction following brain injury. We will also present novel experimental findings, that for the first time, characterize the ex vivo effect of Methylene Blue on mitochondrial function in synaptic and non-synaptic populations of mitochondria.

show abstract

mentioning

confidence: 99%

“…Multiple enzymes that may harm distant organs are also activated [1,2]. Interactions between polymorphonuclear neutrophils and endothelial cells are instrumental in inducing secondary, inflammatory injury to distant organs including lung, heart, kidney and liver and this inflammatory injury is the leading cause of death in critically ill patients [2]. Intestinal I/R is, thus, a common feature of critical care and represents a useful and clinically relevant area of study of the pathophysiological aspects of indirect acute lung injury (ALI) [3].…”

mentioning

confidence: 99%

Reduction of Acute Lung Injury by Administration of Spironolactone After Intestinal Ischemia and Reperfusion in Rats

Barut¹,

Özaçmak²,

TURAN³

et al. 2016

CIM

View full text Add to dashboard Cite

Purpose: Multiple organ failure, including acute lung injury, is a common complication of intestinal ischemia and reperfusion (I/R) injury and contributes to its high mortality rate. Activated polymorphonuclear neutrophils and reactive oxygen species contribute to the lung injury caused by intestinal I/R. Mineralokortikoid receptor antagonist spironolactone has a protective effect against I/R injury in animal models of retina, kidney, heart, and brain. The aim of the present study is to investigate the effect of aldosteron receptor blocker spironolactone on lung injury induced by intestinal I/R.Methods: Wistar albino rats were divided into four groups: (1) sham control; (2) intestinal I/R (30 min of ischemia by superior mesenteric artery occlusion followed by 3 h of reperfusion); (3) spironolactone pretreatment (20 mg/kg) + I/R; and, (4) spironolactone pretreatment without I/R. Spironolactone was given orally 3 days prior to intestinal I/R. A marker for lipid peroxidation (malondialdehyde; MDA), an indicator or oxidation state (reduced glutathione; GSH), an index of polymorphonuclear neutrophil sequestration (myeloperoxidase; MPO), inducible nitric oxide synthase (iNOS) immunoreactivity, and the histopathology of the lung tissue were analyzed.Results: Spironolactone pretreatment markedly reduced intestinal I/R-induced lung injury as indicated by histology and MDA and MPO levels. Moreover, the pretreatment decreased the iNOS immunoreactivity. Conclusion:The present study strongly suggests that spironolactone pretreatment decreased neutrophil infiltration, iNOS induction, oxidative stress, and histopathological injury in an experimental model of intestinal I/R induced-lung injury of rats.

show abstract

Methylene Blue Protects Liver Oxidative Capacity after Gut Ischaemia–Reperfusion in the Rat

Abstract: MB protected against gut IR-induced liver mitochondria dysfunction.

Cited by 23 publications

References 33 publications

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Remote Effects of Lower Limb Ischemia-Reperfusion: Impaired Lung, Unchanged Liver, and Stimulated Kidney Oxidative Capacities

Targeting mitochondrial dysfunction in CNS injury using Methylene Blue; still a magic bullet?

Reduction of Acute Lung Injury by Administration of Spironolactone After Intestinal Ischemia and Reperfusion in Rats

Contact Info

Product

Resources

About