Erythropoietin may attenuate lung inflammation in a rat model of meconium aspiration syndrome

Turhan, Ali Haydar; Atıcı, Aytuğ; Muşlu, Necati; Polat, Ayşe; Sungur, Mehmet Alı

doi:10.1080/01902148.2016.1190424

Cited by 6 publications

(7 citation statements)

References 30 publications

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“…Downstream inflammatory mediators of the TLR4 signaling pathway, including TGF-β1 ( 30 ), TNF-α, IL-6 ( 31 ), IL-1β, IL-17A ( 32 ), MMP-9 and MMP-2 ( 33 ), promote the occurrence and development of MF ( 22 ). In the present study, it was demonstrated that EPO significantly decreased the release of TGF-β1, TNF-α, IL-6, IL-1β and IL-17A in serum and inhibited the expression of MMP-9 and MMP-2 in myocardial tissue of MF in rats subjected to AAC, which was consistent with the findings presented in other reports ( 11 , 34 , 35 ). The effects of EPO on inflammatory mediators may be key in attenuating MF.…”

Section: Discussionsupporting

confidence: 93%

Regulation of TLR4 expression mediates the attenuating effect of erythropoietin on inflammation and myocardial fibrosis in rat heart

et al. 2018

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The mechanism underlying the anti-inflammatory or antifibrotic activity of erythropoietin (EPO) in myocardial fibrosis (MF) remains elusive. In the current study, abdominal aortic constriction (AAC) was performed on rats and EPO and/or Toll-like receptor (TLR)4 were overexpressed in rat hearts through intramyocardial administration of lentivirus expressing the EPO and TLR4 genes. Hematoxylin and eosin staining and Masson's trichrome staining were performed on tissue sections from rat hearts for histopathological examination. ELISA was used to determine the levels of inflammatory mediators in serum. Gene expression levels were determined by quantitative polymerase chain reaction analysis and protein expression levels were determined by western blot analysis and immunofluorescence staining. The results indicated that EPO overexpression improved MF in rat hearts, by inhibiting the release of transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, IL-17A, matrix metalloproteinase (MMP)-9 and MMP-2. Moreover, EPO overexpression suppressed the expression of TLR4, while promoting phosphoinositide 3-kinase (PI3K) and phosphorylated AKT serine/threonine kinase 1 (Akt) expression levels. However, the beneficial effects of EPO were attenuated by overexpression of TLR4. In addition, inhibition of PI3K/Akt signaling activity by treatment with LY294002 markedly reversed the protective effect of EPO on the AAC-induced MF. Taken together, the present study demonstrated that EPO may have a critical role against MF by activating PI3K/Akt signaling and by down-regulating TLR4 expression, thereby inhibiting the release of TGF-β1, TNF-α, IL-6, IL-1β, IL-17A, MMP-9 and MMP-2. These findings suggest that the PI3K/Akt/TLR4 signaling pathway is associated with the anti-inflammatory effects of EPO and may play a role in attenuating AAC-induced MF.

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Section: Discussionsupporting

confidence: 93%

Regulation of TLR4 expression mediates the attenuating effect of erythropoietin on inflammation and myocardial fibrosis in rat heart

et al. 2018

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“…It is reported that 8 hours post the treatment of meconium, approximately 70% apoptotic bodies are found in the airway epithelial cells and the apoptosis is also found in the alveolar epithelial cells [24,25]. In the present study, a MAS model was successfully established on rats, which was verified by the symptoms, such as increased W/D ratio, elevated production of inflammatory factors, and aggravated apoptotic state in the lung tissues, which was consistent with the pathological changes described previously [26,27]. In addition, according to the results of HE staining, significant infiltration of leukocytes and large amounts of alveolar exudates were observed in the lung tissues from MAS rats, which corresponded to the description by Turhan [7].…”

Section: Discussionsupporting

confidence: 91%

Glycyrrhizic acid alleviates the meconium-induced acute lung injury in neonatal rats by inhibiting oxidative stress through mediating the Keap1/Nrf2/HO-1 signal pathway

et al. 2021

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Meconium aspiration syndrome (MAS) is a disease closely related to inflammation and oxidative stress. Glycyrrhizic acid (GA) is a triterpenoid isolated from licorice with multiple bioprotective properties. In the present study, impacts of GA against MAS rats, as well as the potential mechanism, will be investigated. MAS model was established on newborn rats, followed by the treatment of 12.5, 25, and 50 mg/kg GA. The wet/dry weight ratio of lung tissues was calculated. The production of IL-6, IL-1β, TNF-α, malonaldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) was measured using ELISA assay. HE staining was used to evaluate the pathological state of lung tissues and TUNEL assay was used to detect the apoptotic state. The protein expression of Nrf2, Keap1, HO-1, Bcl-2, Bax, and cleaved-Caspase3 was measured by Western blotting assay. The elevated W/D ratio, release of inflammatory factors, lung injury score, and apoptotic index, as well as the activated oxidative stress and suppressed Keap1/Nrf2/HO-1 pathway, in MAS rats were significantly alleviated by GA. After introducing the inhibitor of Nrf2, ML385, the protective property of GA on the pathological state, apoptotic index, and oxidative stress in MAS rats was pronouncedly abolished. Taken together, glycyrrhizin alleviated GAH in rats by suppressing Keap1/Nrf2/HO-1 signaling mediated oxidative stress.

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“…The aim of MAS treatment focuses on minimizing ongoing injury, maintaining oxygenation, and reducing inflammation. Various anti-inflammatory drugs (such as glucocorticoids, phosphodiesterase inhibitors, angiotensin-converting enzyme inhibitors, erythropoietin) have been tested as possible MAS therapies [6][7][8][9] . However, therapy of MAS has controversies to show beneficial effects.…”

Section: ■ Introductionmentioning

confidence: 99%

Effects of hypothermia on lung inflammation in a rat model of meconium aspiration syndrome

2018

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1 2-Experimental SurgeryActa Cir Bras. 2018;33(6):483-490 AbstractPurpose: To evaluate the effects of hypothermia treatment on meconium-induced inflammation. Methods: Fifteen rats were instilled with human meconium (MEC, 1.5 mL/kg, 65 mg/mL) intratracheally and ventilated for 3 hours. Eight rats that were ventilated and not instilled with meconium served as a sham group. In MEC-hypothermia group, the body temperature was lowered to 33±0.5°C. Analysis of the blood gases, interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in bronchoalveolar lavage (BAL) fluid samples, and histological analyses of the lungs were performed. Results: The BAL fluid TNF-α, IL-1β, IL-6 and IL-8 concentrations were significantly higher in the MEC-hypothermia group than in the MEC-normothermia (p < 0.001, p < 0.001, p = 0.001, p < 0.001, respectively) and sham-controlled groups (p < 0.001, p < 0.001, p < 0.001, p < 0.001, respectively). Conclusion: Meconium-induced inflammatory cytokine production is affected by the body temperature control.

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Erythropoietin may attenuate lung inflammation in a rat model of meconium aspiration syndrome

Abstract: rhEPO pretreatment is associated with improved BAL fluid and serum cytokine levels. Pretreatment with rhEPO might reduce the risk of developing of meconium-induced derangements.

Cited by 6 publications

References 30 publications

Regulation of TLR4 expression mediates the attenuating effect of erythropoietin on inflammation and myocardial fibrosis in rat heart

Regulation of TLR4 expression mediates the attenuating effect of erythropoietin on inflammation and myocardial fibrosis in rat heart

Glycyrrhizic acid alleviates the meconium-induced acute lung injury in neonatal rats by inhibiting oxidative stress through mediating the Keap1/Nrf2/HO-1 signal pathway

Effects of hypothermia on lung inflammation in a rat model of meconium aspiration syndrome

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