Characteristics of phosgene aspiration lung injury analyzed based on transcriptomics and proteomics.

Background: Phosgene is a chemical material widely used worldwide. No effective method has been developed to reverse its pathological injuries. Some studies have shown that neuronal inflammation in lung tissue is involved, but the specific mechanism has not been reported.

Early platelet level reduction as a prognostic factor in intensive care unit patients with severe aspiration pneumonia.

This study investigates risk factors underlying the prognosis of severe aspiration pneumonia (SAP) in intensive care unit (ICU) patients and attempts to provide early prognosis reference for clinical tasks. Patients diagnosed with SAP and admitted to the ICU of Jinshan Hospital, Fudan University, Shanghai, China, between January 2021 and December 2021 were recruited in this retrospective cohort study. Clinical data on a patient's general condition, underlying diseases, laboratory indicators, and 90-day outcomes (survival or death) were recorded.

NLRP3 gene silencing ameliorates phosgene-induced acute lung injury in rats by inhibiting NLRP3 inflammasome and proinflammatory factors, but not anti-inflammatory factors.

NOD-like receptor protein 3 (NLRP3) is involved in acute lung injury (ALI), but its exact role in phosgene-induced ALI is not clearly understood. The aim of the study is to explore the potential therapeutic effect of NLRP3 inflammasome modulation in the management of phosgene-induced ALI. ALI was induced in rats by phosgene exposure at 8.

Adenovirus-delivered angiopoietin-1 ameliorates phosgene-induced acute lung injury via inhibition of NLRP3 inflammasome activation.

Objective: Angiopoietin-1 (Ang1) is reported to have the ability to attenuate endothelial permeability and inflammation during the stress condition and is considered to play a critical role in vascular stabilization. The aim of this study was to investigate the mechanisms involved in the protective effects of adenovirus-delivered Ang1 in phosgene-induced acute lung injury (ALI).

Methods: ALI was induced in rats by phosgene exposure at 8.

Adenovirus-delivered angiopoietin-1 suppresses NF-κB and p38 MAPK and attenuates inflammatory responses in phosgene-induced acute lung injury.

Animals exposed to phosgene (Psg) result in acute lung injury (ALI). We have recently reported that angiopoietin-1 (Ang1) reduces inflammation and vascular hyperpermeability in ALI animals. In this study, we examined whether the beneficial effects of adenovirus-delivered Ang1 (Ad/Ang1) on inflammatory responses in Psg-induced ALI rats are due to the suppression of the nuclear factor-kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) pathways, which play crucial roles in inflammatory responses in ALI.

[Effects of phosphorylated mitogen-activated protein kinases on phosgene inhalation-induced lung injury in rats and its relationship with matrix metalloproteinase].

Objective: To investigate the effects of phosphorylated mitogen-activated protein kinases (MAPK), including the phosphorylated extracellular signal-regulated protein kinase 1/2 (p-ERK1/2), the phosphorylated protein p38 (p-p38), the phosphorylated c-Jun N-terminal kinase (p-JNK), on phosgene inhalation-induced lung injury and its relationship with matrix metalloproteinase 9 (MMP-9).

Methods: According to the random number table, 30 male Wistar rats were divided into air control group (C), phosgene inhalation group (P), PD98059 (specific inhibitor of ERK1/2) group, SB203580 (specific inhibitor of p38) group, and SP600125 (specific inhibitor of JNK) group, with 6 rats in each group. The number of neutrophils in the bronchoalveolar lavage fluid (BALF) was counted and the lung wet-dry ratio (W/D) was examined.

Adenovirus-delivered angiopoietin-1 treatment for phosgene-induced acute lung injury.

Context: Exposure to phosgene can result in an acute lung injury, leading to pulmonary edema and even death. Angiopoietin-1 (Ang1) is a critical factor for vascular stabilization due to its ability to reduce endothelial permeability and inflammation.

Objective: In this study, the histopathological changes of the lungs after exposure to phosgene and the effect of Ang1 treatment were examined.

[Protective effect of melatonin in rats with phosgene-induced lung injury].

Objective: To investigate the antioxidant effect of melatonin (MT) in the rats with phosgene-induced lung injury and its possible mechanism.

Methods: Fifty male SD rats were equally randomized into phosgene exposure group, air control group, MT treatment group, dexamethasone (DX) treatment group, and negative control group. All groups except the air control group were exposed to 8.

[Expression and role of mitogen activated protein kinases signaling pathway in lung injury induced by phosgene].

Objective: This study aimed to investigate the expression and role of the mitogen activated protein kinases (ERK1/2, P38, JNK) in phosgene induced lung injury in rats in vivo.

Method: 30 male wistar rats were randomized into the group as follows, Gas inhalation control group, Phosgene inhalation group, and the following groups of the inhibitors of MAPK, involving SP600125, PD98059 and SB203580, 6 animals in each group, we copy the model of phosgene-induced lung injury, used the directional flow-inhalation device, the air control group inhaled the air, and the intervention groups were given PD98059 (intraperitoneal injection), SB203580 (hypodermic injection), SP600125 (intravenous) respectively before the inhalation of phosgene. The locations and quantities of three subfamilies of MAPKs (ERK1/2, P38, JNK) and p-MAPKs (p-ERK1/2, p-P38, p-JNK) were analyzed by immunohistochemistry and Western Blot analysis respectively; The histopathological changes of lung tissues, the number of neutrophil cells and the W/D were examined.

[Effects of dexamethasone pretreatment on expression of matrix metalloproteinase-9 in rats with acute lung injury induced by phosgene].

Objective: To investigate the effects of dexamethasone on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute lung injury induced by phosgene.

Methods: The rats were randomly divided into 3 groups: normal control group that consists of the rats with air exposure, phosgene group that consists of the rats with phosgene exposure and dexamethasone group that consists of the rats with phosgene exposure after 2.5 mg/kg dexamethasone being injected.

[Protective effects of ulinastatin on phosgene-induced acute lung injury and relation to matrix metalloproteinase-9].

Objective: To observe the protective mechanism of ulinastatin on mice with acute lung injury induced by exposure to phosgene and its relationship to the expressions of matrix metalloproteinase-9 (MMP-9) in the lung tissues.

Methods: Sixty-four healthy male SD rats were randomly divided into two groups: the experimental group and the control group. 32 rats in the experiment group were randomly subdivided into four groups: rats with phosgene exposure group, rats with phosgene exposure after saline injected group, rats with phosgene exposure after dexamethasone injected group.