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      Penehyclidine hydrochloride alleviates lipopolysaccharide-induced acute respiratory distress syndrome in cells via regulating autophagy-related pathway

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          Abstract

          Acute progressive hypoxic respiratory failure caused by various predisposing factors is known as acute respiratory distress syndrome (ARDS). Although penehyclidine hydrochloride (PHC), an anticholinergic drug, is widely applied in clinical practice, the specific mechanisms underlying PHC in the treatment of ARDS are not completely understood. In the present study, BEAS-2B cells were treated with 10 ng/ml lipopolysaccharide (LPS) to establish an ARDS cell model and a rat model of acute lung injury (ALI). The influences of PHC and/or autophagy inhibitor (3-methyladenine (3-MA)) on the morphology, autophagy, proliferation and apoptosis of cells and tissues were evaluated using hematoxylin and eosin staining, Cell Counting Kit-8 assays, Hoechst staining, TUNEL staining, flow cytometry, immunofluorescence assays, ELISAs and scanning electron microscopy. The expression levels of apoptosis- and autophagy-related proteins were measured via western blotting. The results indicated that PHC enhanced proliferation and autophagy, and decreased apoptosis and the inflammatory response in LPS-induced BEAS-2B cells and ALI model rats. In addition, 3-MA reversed the effects of PHC on proliferation, inflammation, apoptosis and autophagy in LPS-induced BEAS-2B cells. Therefore, the present study suggested that PHC demonstrated a protective effect in LPS-induced ARDS by regulating an autophagy-related pathway.

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          Most cited references60

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          Activation of apoptosis signalling pathways by reactive oxygen species.

          Reactive oxygen species (ROS) are short-lived and highly reactive molecules. The generation of ROS in cells exists in equilibrium with a variety of antioxidant defences. At low to modest doses, ROS are considered to be essential for regulation of normal physiological functions involved in development such as cell cycle progression and proliferation, differentiation, migration and cell death. ROS also play an important role in the immune system, maintenance of the redox balance and have been implicated in activation of various cellular signalling pathways. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles, which can lead to activation of cell death processes such as apoptosis. Apoptosis is a highly regulated process that is essential for the development and survival of multicellular organisms. These organisms often need to discard cells that are superfluous or potentially harmful, having accumulated mutations or become infected by pathogens. Apoptosis features a characteristic set of morphological and biochemical features whereby cells undergo a cascade of self-destruction. Thus, proper regulation of apoptosis is essential for maintaining normal cellular homeostasis. ROS play a central role in cell signalling as well as in regulation of the main pathways of apoptosis mediated by mitochondria, death receptors and the endoplasmic reticulum (ER). This review focuses on current understanding of the role of ROS in each of these three main pathways of apoptosis. The role of ROS in the complex interplay and crosstalk between these different signalling pathways remains to be further unravelled during the coming years.
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            Acute Respiratory Distress Syndrome

            Acute respiratory distress syndrome (ARDS) is a life-threatening form of respiratory failure that affects approximately 200 000 patients each year in the United States, resulting in nearly 75 000 deaths annually. Globally, ARDS accounts for 10% of intensive care unit admissions, representing more than 3 million patients with ARDS annually.
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              The acute respiratory distress syndrome: pathogenesis and treatment.

              The acute respiratory distress syndrome (ARDS) causes 40% mortality in approximately 200,000 critically ill patients annually in the United States. ARDS is caused by protein-rich pulmonary edema that causes severe hypoxemia and impaired carbon dioxide excretion. The clinical disorders associated with the development of ARDS include sepsis, pneumonia, aspiration of gastric contents, and major trauma. The lung injury is caused primarily by neutrophil-dependent and platelet-dependent damage to the endothelial and epithelial barriers of the lung. Resolution is delayed because of injury to the lung epithelial barrier, which prevents removal of alveolar edema fluid and deprives the lung of adequate quantities of surfactant. Lymphocytes may play a role in resolution of lung injury. Mortality has been markedly reduced with a lung-protective ventilatory strategy. However, there is no effective pharmacologic therapy, although cell-based therapy and other therapies currently being tested in clinical trials may provide novel treatments for ARDS.
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                Author and article information

                Journal
                Mol Med Rep
                Mol Med Rep
                Molecular Medicine Reports
                D.A. Spandidos
                1791-2997
                1791-3004
                February 2021
                01 December 2020
                01 December 2020
                : 23
                : 2
                : 100
                Affiliations
                Department of Pediatrics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China
                Author notes
                Correspondence to: Dr Liangxia Wu, Department of Pediatrics, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 600 Yishan Road, Xuhui, Shanghai 200233, P.R. China, E-mail: wuliangxia6@ 123456126.com
                Article
                MMR-0-0-11739
                10.3892/mmr.2020.11739
                7723159
                33300058
                2e9a79f0-c004-42a9-b187-408cfced5c8b
                Copyright: © Wang et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 27 July 2019
                : 30 April 2020
                Categories
                Articles

                penehyclidine hydrochloride,autophagy,acute respiratory distress syndrome,lipopolysaccharide,apoptosis

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