Insulin attenuates endotoxin-induced acute lung injury in conscious rats

Chen, Hsing I.; Yeh, Diana; Liou, Huey-Ling; Kao, Shu Huei

doi:10.1097/01.ccm.0000201902.37115.22

Cited by 66 publications

(57 citation statements)

References 49 publications

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“…ALI is a life-threatening disease that often leads to acute hypoxemic respiratory failure with intensive pulmonary inflammation, accompanied by various cellular and molecular changes [23,24] . The pathogenesis of endotoxin-induced ALI remains obscure and has not yet been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Huang

Liu

et al. 2012

Acta Pharmacol Sin

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Section: Discussionmentioning

confidence: 99%

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Huang

Liu

et al. 2012

Acta Pharmacol Sin

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“…Studies from the present authors' laboratory have investigated the pathogenic mechanisms and potential therapeutic regimen on ALI induced by endotoxin [12,13] and I/R [3,4]. The present study was designed to evaluate the protective effect of nicotinamide on ALI caused by I/R in isolated perfused lungs.…”

mentioning

confidence: 99%

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Su¹,

Liu²,

Kao³

et al. 2007

European Respiratory Journal

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Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung injury and associated alterations following ischaemia/reperfusion (I/R) of the isolated perfused rat's lung.I/R increased the lung weight (LW) to body weight ratio, LW gain, protein and dye tracer leakage, pulmonary arterial pressure and capillary permeability. The insult also increased nitrate/ nitrite, methyl guanidine, tumour necrosis factor-a and interleukin-1b in lung perfusate, while it decreased adenosine triphosphate content with an increase in PARP activity in lung tissue.Most of the I/R-induced changes were abrogated by post-treatment (30 min after I/R) with nicotinamide (100 mg?kg -1 body weight). However, the increase in pulmonary arterial pressure was enhanced by nicotinamide post-treatment. Following I/R, the inducible nitric oxide synthase (iNOS) mRNA expression was enhanced. Nicotinamide reduced the iNOS expression. The results suggest that nicotinamide exerted a protective effect on the acute lung injury caused by ischaemia/reperfusion. The mechanisms may be mediated through the inhibition on the poly (adenosine diphosphate-ribose) polymerase activity, inducible nitric oxide synthase expression and the subsequent suppression of nitric oxide, free radicals and pro-inflammatory cytokines with restoration of adenosine triphosphate.

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“…The samples were centrifuged at 3,000 g for 10 mins. The supernatant was used for determination of nitrate/nitrite with high-performance chromatography [23,24]. The formation of methyl guanidine (MG) has been identified as an index of hydroxyl radical production [25].…”

Section: Methodsmentioning

confidence: 99%

Niacinamide mitigated the acute lung injury induced by phorbol myristate acetate in isolated rat's lungs

et al. 2012

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BackgroundPhorbol myristate acetate (PMA) is a strong neutrophil activator and has been used to induce acute lung injury (ALI). Niacinamide (NAC) is a compound of B complex. It exerts protective effects on the ALI caused by various challenges. The purpose was to evaluate the protective effects of niacinamide (NAC) on the PMA-induced ALI and associated changes.MethodsThe rat's lungs were isolated in situ and perfused with constant flow. A total of 60 isolated lungs were randomized into 6 groups to received Vehicle (DMSO 100 μg/g), PMA 4 μg/g (lung weight), cotreated with NAC 0, 100, 200 and 400 mg/g (lung weight). There were 10 isolated lungs in each group. We measured the lung weight and parameters related to ALI. The pulmonary arterial pressure and capillary filtration coefficient (Kfc) were determined in isolated lungs. ATP (adenotriphosphate) and PARP [poly(adenosine diphophate-ribose) polymerase] contents in lung tissues were detected. Real-time PCR was employed to display the expression of inducible and endothelial NO synthases (iNOS and eNOS). The neutrophil-derived mediators in lung perfusate were determined.ResultsPMA caused increases in lung weight parameters. This agent produced pulmonary hypertension and increased microvascular permeability. It resulted in decrease in ATP and increase in PARP. The expression of iNOS and eNOS was upregulated following PMA. PMA increased the neutrophil-derived mediators. Pathological examination revealed lung edema and hemorrhage with inflammatory cell infiltration. Immunohistochemical stain disclosed the presence of iNOS-positive cells in macrophages and endothelial cells. These pathophysiological and biochemical changes were diminished by NAC treatment. The NAC effects were dose-dependent.ConclusionsOur results suggest that neutrophil activation and release of neutrophil-derived mediators by PMA cause ALI and associated changes. NO production through the iNOS-producing cells plays a detrimental role in the PMA-induced lung injury. ATP is beneficial, while PARP plays a deteriorative effect on the PMA-induced ALI. NAC exerts protective effects on the inflammatory cascade leading to pulmonary injury. This B complex compound may be applied for clinical usage and therapeutic regimen.

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Insulin attenuates endotoxin-induced acute lung injury in conscious rats

Abstract: Insulin is effective in reducing or preventing the lipopolysaccharide-induced increases in plasma nitrate/nitrite and methyl guanidine and the occurrence of acute lung injury.

Cited by 66 publications

References 49 publications

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Niacinamide mitigated the acute lung injury induced by phorbol myristate acetate in isolated rat's lungs

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