Protein S is Protective in Acute Lung Injury by Inhibiting Cell Apoptosis

Abstract

Acute lung injury is a fatal disease characterized by inflammatory cell infiltration, alveolar-capillary barrier disruption, protein-rich edema, and impairment of gas exchange. Protein S is a vitamin K-dependent glycoprotein that exerts anticoagulant, immunomodulatory, anti-inflammatory, anti-apoptotic, and neuroprotective effects. The aim of this study was to evaluate whether human protein S inhibits cell apoptosis in acute lung injury. Acute lung injury in human protein S transgenic and wild-type mice was induced by intratracheal instillation of lipopolysaccharide. The effect of human protein S on apoptosis of lung tissue cells was evaluated by Western blotting. Inflammatory cell infiltration, alveolar wall thickening, myeloperoxidase activity, and the expression of inflammatory cytokines were reduced in human protein S transgenic mice compared to the wild-type mice after lipopolysaccharide instillation. Apoptotic cells and caspase-3 activity were reduced while phosphorylation of extracellular signal-regulated kinase was enhanced in the lung tissue from human protein S transgenic mice compared to wild-type mice after lipopolysaccharide instillation. The results of this study suggest that human protein S is protective in lipopolysaccharide-induced acute lung injury by inhibiting apoptosis of lung cells.

Honokiol alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via Nrf2 activation in vitro and in vivo

“…The rats were randomly divided into six groups (n = 8): control group, LPS group, LPS + HKL groups (1.25, 2.5, 5 mg/kg), LPS + HKL (2.5 mg/kg) + ML385 (30 mg/kg) group. Firstly, the rats were anesthetized by injecting sodium pentobarbital (50 mg/kg) intraperitoneally, followed by subsequent intratracheal instillation of 5 mg/kg LPS in 50 μl of sterile phosphate-buffered saline (PBS) [ 19 ], while the control group was administrated with an equal volume of PBS. Half an hour after LPS administration, the rats were injected intraperitoneally with HKL (1.25, 2.5, 5 mg/kg) [ 20 ] dissolved in DMSO, while the control group was treated with PBS alone.…”

Regulation of PINX1 expression ameliorates lipopolysaccharide-induced lung injury and alleviates cell senescence during the convalescent phase through affecting the telomerase activity

“…Extensive lung inflammation contributes to the destruction of the basement membrane and increased the permeability of the alveolar-capillary membrane [ 18 ]. Numerous studies unveil that an exaggerated inflammatory response can cause apoptosis, which plays a vital role in the pathogenesis of ALI [ 19 , 20 ]. Accumulation of a mass of inflammatory factors in lung tissues has been demonstrated to lead to pulmonary cell apoptosis [ 21 ].…”

6-Gingerol attenuates sepsis-induced acute lung injury by suppressing NLRP3 inflammasome through Nrf2 activation

“…The rats were divided into 4 groups (n = 8 each): control group, LPS group, LPS + 6-Gingerol (20 mg/kg) group, and LPS + 6-Gingerol + ML385 (30 mg/kg) group. Rats were intraperitoneally injected with 50 mg/kg sodium pentobarbital for anesthesia, and then they were subjected to intratracheal instillation of 5 mg/kg LPS in 50 μL PBS [32]. The control rats received an equal volume of PBS.…”