Beraprost sodium, a prostacyclin (PGI) analogue, ameliorateslipopolysaccharide-induced cellular injury in lung alveolar epithelial cells

Vicil, Sinan; Erdoğan, Suat

doi:10.3906/sag-1401-108

Cited by 4 publications

(3 citation statements)

References 46 publications

(75 reference statements)

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“…Br, bronchiole; PA, pulmonary artery. dation and prevent depletion of cellular antioxidants in lipopolysaccharide-induced injury to alveolar epithelial cells (52). Beraprost also inhibits cigarette smoke extract-induced emphysema in rats by attenuating apoptosis, inhibiting proteolytic enzymes, and augmenting antioxidants in addition to reducing inflammatory cytokines (15).…”

Section: Discussionmentioning

confidence: 99%

Iloprost attenuates hyperoxia-mediated impairment of lung development in newborn mice

Olave

Lal

Halloran

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Cyclooxygenase-2 (COX-2/PTGS2) mediates hyperoxia-induced impairment of lung development in newborn animals and is increased in the lungs of human infants with bronchopulmonary dysplasia (BPD). COX-2 catalyzes the production of cytoprotective prostaglandins, such as prostacyclin (PGI), as well as proinflammatory mediators, such as thromboxane A2. Our objective was to determine whether iloprost, a synthetic analog of PGI, would attenuate hyperoxia effects in the newborn mouse lung. To test this hypothesis, newborn C57BL/6 mice along with their dams were exposed to normoxia (21% O) or hyperoxia (85% O) from 4 to 14 days of age in combination with daily intraperitoneal injections of either iloprost 200 µg·kg·day, nimesulide (selective COX-2 antagonist) 100 mg·kg·day, or vehicle. Alveolar development was estimated by radial alveolar counts and mean linear intercepts. Lung function was determined on a flexiVent, and multiple cytokines and myeloperoxidase (MPO) were quantitated in lung homogenates. Lung vascular and microvascular morphometry was performed, and right ventricle/left ventricle ratios were determined. We determined that iloprost (but not nimesulide) administration attenuated hyperoxia-induced inhibition of alveolar development and microvascular density in newborn mice. Iloprost and nimesulide both attenuated hyperoxia-induced, increased lung resistance but did not improve lung compliance that was reduced by hyperoxia. Iloprost and nimesulide reduced hyperoxia-induced increases in MPO and some cytokines (IL-1β and TNF-α) but not others (IL-6 and KC/Gro). There were no changes in pulmonary arterial wall thickness or right ventricle/left ventricle ratios. We conclude that iloprost improves lung development and reduces lung inflammation in a newborn mouse model of BPD.

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Section: Discussionmentioning

confidence: 99%

Iloprost attenuates hyperoxia-mediated impairment of lung development in newborn mice

Olave

Lal

Halloran

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Accumulating evidence has demonstrated that PGI 2 has the ability to suppress the expression of TNF-α. For instances, Vicil et al [ 24 ] reported that TNF-α synthesis was inhibited by the PGI 2 analogue beraprost sodium in lipopolysaccharide (LPS)-treated lung alveolar epithelial cells. In line with this observation, Yeh et al [ 25 ] found that PGI 2 analogues, including iloprost and treprostinil, suppressed LPS-induced TNF-α expression in human monocyte-derived dendritic cells.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin I2 is responsible for ameliorating prostaglandin E2 stress in stimulating the expression of tumor necrosis factor α in a β-amyloid protein -dependent mechanism

et al. 2017

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Cyclooxygenase-2 (COX-2) has been found to be induced during the early stage of Alzheimer’s disease (AD). Using mouse-derived astrocyte and APP/PS1 transgenic (Tg) mice as model systems, we firstly elucidated the mechanisms underlying COX-2 metabolic production including prostaglandin (PG)E2- and PGI2-mediated tumor necrosis factor α (TNF-α) regulation. Specifically, PGE2 accumulation in astrocyte activated the p38 and JNK/c-Jun signaling pathways via phosphorylation, resulting in TNF-α expression. In contrast, the administration of PGI2 attenuated the effects of PGE2 in stimulating the production of TNF-α by inhibiting the activity of TNF-α promoter and the binding activity of AP1 on the promoter of TNF-α. Moreover, our data also showed that not only Aβ1-42 oligomers but also Aβ1-42 fibrils have the ability to involve in mediating the antagonistic effects of PGE2 and PGI2 on regulating the expression of TNF-α via a p38- and JNK/c-Jun-dependent, AP1-transactivating mechanism. Reciprocally, the production of TNF-α finally accelerated the deposition of β-amyloid protein (Aβ)1-42 in β-amyloid plaques (APs), which contribute to the cognitive decline of AD.

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“…Beraprost sodium (BPS) is an analog of prostacyclin that has a longer half-life, more stable chemical characteristics, and higher oral bioavailability 22. Apart from its arterial vasodilative and antiplatelet effects,23,24 BPS properties including anti-inflammatory and antioxidant activities have also been investigated 25–32. Blocking or inhibiting inflammatory cascades or oxidative stress has been demonstrated to protect against cell death in hepatic IR injury 33,34.…”

Section: Introductionmentioning

confidence: 99%

Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways

Deng¹,

Jiao²,

Liu³

et al. 2018

DDDT

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ObjectiveThe goal of this study was to determine the effects of beraprost sodium (BPS) preconditioning on hepatic ischemia-reperfusion (IR) injury and its underlying mechanisms of action.Materials and methodsMice were randomly divided into sham, IR, IR+BPS (50 µg/kg), and IR+BPS (100 µg/kg) groups. Saline or BPS was given to the mice by daily gavage for 1 week before the hepatic IR model was established. Liver tissues and orbital blood were collected at 2, 8, and 24 hours after reperfusion for the determination of liver enzymes, inflammatory mediators, apoptosis- and autophagy-related proteins, key proteins in P38 and c-Jun N-terminal kinase (JNK) cascades, and evaluation of liver histopathology.ResultsBPS preconditioning effectively reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, improved pathological damage, ameliorated production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and affected expressions of Bax, Bcl-2, Caspase-3, Caspase-8, and Caspase-9, microtubule-associated protein 1 light chain 3 (LC3), Beclin-1, and P62. The protective effects of BPS preconditioning were associated with reduced P38 and JNK phosphorylation.ConclusionBPS preconditioning ameliorated hepatic IR injury by suppressing inflammation, apoptosis, and autophagy, partially via inhibiting activation of the P38 and JNK cascades.

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Beraprost sodium, a prostacyclin (PGI) analogue, ameliorateslipopolysaccharide-induced cellular injury in lung alveolar epithelial cells

Cited by 4 publications

References 46 publications

Iloprost attenuates hyperoxia-mediated impairment of lung development in newborn mice

Iloprost attenuates hyperoxia-mediated impairment of lung development in newborn mice

Prostaglandin I2 is responsible for ameliorating prostaglandin E2 stress in stimulating the expression of tumor necrosis factor α in a β-amyloid protein -dependent mechanism

Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways

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