Pioglitazone attenuates lung injury by modulating adipose inflammation

Kutsukake, Masahiko; Matsutani, Takeshi; Tamura, Kazuhiro; Matsuda, Akihisa; Kobayashi, Makoto; Tachikawa, Eiichi; Uchida, Eiji

doi:10.1016/j.jss.2014.03.007

Cited by 37 publications

(41 citation statements)

References 32 publications

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“…The association of pioglitazone in patients' therapy in ICU reduces significantly the complication that can arise from lung injuries. These effects have been studied by Kutsukake et al [93], demonstrating that through the administration of this active compound the tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) concentrations (Fig. 2) are significantly reduced, and also haemocyte infiltration, inflammation and cellular death is reduced (Fig.…”

Section: Therapy With Antioxidantsmentioning

confidence: 78%

“…2) are significantly reduced, and also haemocyte infiltration, inflammation and cellular death is reduced (Fig. 3) [93]. The levels of pro-inflammatory cytokines that are released uncontrollably in the pulmonary tissue are also inhibited by ulistatin [110] or salidroside [111].…”

Section: Therapy With Antioxidantsmentioning

confidence: 87%

“…In many scientific papers the beneficial effect of the sulphureted hydrogen on the inflammated lung is presented [88,[93][94][95][96][97]. Benetti et al [88] demonstrates that through the administration of the sodium mono-hydrogen-sulphate (NaHS) that generates sulphureted hydrogen, the accumulation of neutrophils and of eosinophils is inhibited.…”

Section: Therapy With Antioxidantsmentioning

confidence: 99%

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Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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Multiple trauma patients require extremely good management and thus, the trauma team needs to be prepared and to be up to date with the new standards of intensive therapy. Oxidative stress and free radicals represent an extremely aggressive factor to cells, having a direct consequence upon the severity of lung inflammation. Pulmonary tissue is damaged by oxidative stress, leading to biosynthesis of mediators that exacerbate inflammation modulators. The subsequent inflammation spreads throughout the body, leading most of the time to multiple organ dysfunction and death. In this paper, we briefly present an update of biochemical effects of oxidative stress and free radical damage to the pulmonary tissue in patients in critical condition in the intensive care unit. Also, we would like to present a series of active substances that substantially reduce the aggressiveness of free radicals, increasing the chances of survival.

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Section: Therapy With Antioxidantsmentioning

confidence: 78%

Section: Therapy With Antioxidantsmentioning

confidence: 87%

Section: Therapy With Antioxidantsmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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“…For example, epithelial type II cells showed a significant increase in apoptosis in animal models of LPS-induced acute lung injury (Kitamura et al, 2001). Given the growing body of evidence that epithelial cell apoptosis is known to be pivotal contributor to pathogenesis of sepsis-induced lung injury (Kutsukake et al, 2014;Imazu et al, 2011). At present study, LPS-induced primary cultured rat AEC II cell death was investigated.…”

Section: Discussionmentioning

confidence: 93%

Apoptosis and surfactant protein-C expression inhibition induced by lipopolysaccharide in AEC II cell may associate with NF-κB pathway

et al. 2017

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-Lipopolysaccharide (LPS), a Gram-negative bacterial outer membrane component, is one of the major causes of septic shock. Herein we investigate LPS-induced apoptosis of rat alveolar epithelial type II cells (AEC II) and the effects of LPS on surfactant protein-C (SP-C) expression in AEC II, along with the possible molecular mechanisms. LPS exposure impaired cell viability and increased apoptosis of AEC II significantly in concentration-dependent manner embodied in increased caspase-3 expression and the activity of caspase-3. Simultaneously, our results also indicated that LPS inhibited surfactant protein-C (SP-C) expression in AEC II. Mechanistic studies revealed that LPS treatment significantly increased the expression of NF-κB p50, NF-κB p65 and IKKβ proteins as well as induced IκB-α phosphorylation. Moreover, pretreatment with IKK inhibitor IKK-16 or NF-κB inhibitor PDTC ameliorated LPScaused alterations in cleaved caspase-3 expression, the activity of caspase-3 and SP-C expression. Taken together, these results demonstrate that LPS can induce apoptosis of AEC II and decrease SP-C expression partly through activating the NF-κB pathway.

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“…10,18) Low preoperative circulating levels of adiponectin might be a risk factor for postoperative infection in patients who undergo colorectal cancer surgery.…”

Section: Discussionmentioning

confidence: 99%

Impact of Pioglitazone on Macrophage Dynamics in Adipose Tissues of Cecal Ligation and Puncture-Treated Mice

Matsutani

Tamura

Kutsukake

et al. 2017

Biological & Pharmaceutical Bulletin

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Pioglitazone improves sepsis-induced organ injury accompanied with anti-inflammatory effects on visceral adipose tissue. However, its action in adipose immune cells remains to be ascertained. We investigated the effects of pioglitazone on visceral adipose macrophage population and polarisation in cecal ligation and puncture (CLP)-induced sepsis mice. Eight-week-old male mice were assigned to 3 groups: 1) sham-operated group, 2) CLP group, or 3) pioglitazone-treated CLP group. Pioglitazone (10 mg/kg) was injected intraperitonally for 7 d and CLP surgery was performed. Visceral adipose tissues were collected 24 h after the surgery. mRNA expression of several macrophage markers (inducible nitric oxide synthase (iNOS) for M1, arginase1

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Pioglitazone attenuates lung injury by modulating adipose inflammation

Cited by 37 publications

References 32 publications

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Apoptosis and surfactant protein-C expression inhibition induced by lipopolysaccharide in AEC II cell may associate with NF-κB pathway

Impact of Pioglitazone on Macrophage Dynamics in Adipose Tissues of Cecal Ligation and Puncture-Treated Mice

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