الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Starting in China, the novel 2019 coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) showed a rapid incidence around the world. SARS-COV-2-infected patients with severe pneumonia rapidly develop acute respiratory distress syndrome (ARDS) and die of multiple organ failure. Despite advances in supportive care approaches, ARDS is still associated with high mortality and morbidity among those patients (Qin and Zhao, 2020) Acute respiratory distress syndrome (ARDS) is one of the severe complications of acute lung injury (ALI) which remains a major cause of morbidity and mortality in critically ill patients with ALI. Acute pulmonary inflammatory response is a criterion of ALI/ARDS. They are related to numerous clinical conditions, for instance pneumonia, interstitial edema, sepsis, and the new coronavirus disease (COVID-19) which caused by severe acute respiratory syndrome coronavirus 2 (SARS-COV-2). The latter rapidly develop ARDS and cause patients death of multiple organ failure Apoptosis or programmed cell death is another mechanism, which is involved in the pathogenesis of induced lung injury. In the current study, we found up-regulation of caspase-3 with down-regulation of BCl2 in lung tissues at the levels of mRNA suggesting activation of apoptotic process in induced lung injury Treatment with MSCs or CoPP resulted in significant reductions in lung tissue damage score, MDA, caspase-3, serum TNF-α levels with significant elevations in BCl2, SOD, CAT and Hb contents. The present study suggests that MSCs and CoPP could attenuate ALI via modulation of inflammation, oxidative stress, and apoptosis. MSCs action was more effective than CoPP.