Clinical implications of Golgi protein 73 and granulocyte colony-stimulating factor and their related factors in children with bronchopneumonia

Li, Baofa; Liu, Xin

doi:10.1016/j.jped.2022.05.005

Cited by 1 publication

(2 citation statements)

References 26 publications

(25 reference statements)

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“…The excessive activation of inflammatory response is one of the important pathophysiological changes during the occurrence and development of bronchopneumonia (Kylat, 2021). The excess release of inflammatory cytokines will damage the alveolar epithelial cells and capillary endothelial cells, which thus affects the alveolar ventilation function, finally inducing hypoxemia (Li & Liu, 2022; Liu, Carlisle, et al., 2021). Moreover, the excessively released inflammatory cytokines will enter the blood circulation, causing the activation of systemic inflammatory response, and multiple organ dysfunction (Li & Liu, 2022; Liu, Carlisle, et al., 2021).…”

Section: Discussionmentioning

confidence: 99%

“…The excess release of inflammatory cytokines will damage the alveolar epithelial cells and capillary endothelial cells, which thus affects the alveolar ventilation function, finally inducing hypoxemia (Li & Liu, 2022; Liu, Carlisle, et al., 2021). Moreover, the excessively released inflammatory cytokines will enter the blood circulation, causing the activation of systemic inflammatory response, and multiple organ dysfunction (Li & Liu, 2022; Liu, Carlisle, et al., 2021). Moreover, we found that Remimazolam reduced inflammation in vitro model.…”

Section: Discussionmentioning

confidence: 99%

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Remimazolam attenuates inflammation in bronchopneumonia through the inhibition of NLRP3 activity by PDPK1 ubiquitination

Yang,

2024

Chem Biol Drug Des

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Bronchopneumonia is the most common pneumonia in childhood. Therefore, we tested the effects of Remimazolam presented Bronchopneumonia and its possible mechanisms. Phillygenin increased survival rate, reduced W/D ratio, and lung injury score, and inhibited IL‐1β, IL‐6, TNF‐α, and INF‐γ levels in mice model of bronchopneumonia. Remimazolam induced PDPK1 and p‐AKT protein expressions, and suppressed NLRP3 protein expression in lung tissue of mice model. In vitro model, Remimazolam also induced PDPK1 and p‐AKT protein expressions, and suppressed NLRP3 protein expression. Remimazolam also inhibited inflammation levels in vitro model. PDPK1 inhibitor, PHT‐427 (100 mg/kg) reduced survival rate, increased W/D ratio and lung injury score, and promoted inflammation levels in mice model of bronchopneumonia by treated with Remimazolam. PHT‐427 suppressed PDPK1 and p‐AKT protein expressions and induced NLRP3 protein expression in mice model of bronchopneumonia by treated with Remimazolam. Remimazolam interlinked PDPK1 protein. Remimazolam increased the expressions of PDPK1 and p‐AKT in vitro model. Remimazolam reduced PDPK1 ubiquitination in vitro model.

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