Rationale: The cystic features of the novel coronavirus disease 2019 (COVID-19) found on computed tomography (CT) have not yet been reported in the published literature. We report the cystic chest CT findings of 2 patients confirmed to have COVID-19-related pneumonia. Patient concerns: A 38-year-old man and a 35-year-old man diagnosed with severe COVID-19 pneumonia were admitted to the intensive care unit. Diagnoses: Chest CT findings showed multiple cysts in ground-glass opacities (bilaterally) with/without pneumothorax. The cysts had a smooth inner wall. Interventions: The patients continued to be given oxygen by mask and received antitussive, phlegm-dispelling treatment. Outcomes: At follow up, there was a reduction in the number of multiple cystic lesions on CT. To date, 1 patient was discharged from hospital, while the other had been transferred to the rehabilitation department. Lessons: COVID-19 may independently result in pulmonary cyst formation and pneumothorax; the application of a ventilator may be another causative factor.

Antioxidative therapy is considered an effective strategy for treating oxidative stress-induced apoptosis in cardiovascular diseases. Salidroside has been used as an antioxidative therapy for oxidative injury in cardiac diseases. However, the mechanism underlying its antioxidant effect is poorly understood. The present study aimed to investigate the pharmacological effects of salidroside on cultured human umbilical vein endothelial cells (HUVECs) under conditions of oxidative injury induced by hydrogen peroxide (H2O2) and the underlying mechanisms in vitro. HUVECs pretreated with or without salidroside for 24 h were exposed to H2O2-induced oxidative stress conditions for 6 h and then cell viability, apoptosis, HIF-1α, regulated in development and DNA damage responses-1 (REDD1) and the PI3K/Akt/mTOR pathway were investigated. The results demonstrated that salidroside effectively attenuated H2O2-impaired cell viability and the production of reactive oxygen species (ROS) in a concentration-dependent manner. Reduced H2O2-induced apoptosis and activation of the cellular PI3K/Akt/mTOR pathway were demonstrated in HUVECs pretreated with salidroside. Furthermore, the level of REDD1, a direct regulator of mitochondrial metabolism, significantly increased in parallel with the level of HIF-1α following pretreatment with salidroside. The antioxidative effect of salidroside was abrogated in REDD1 knockdown cells. However, LY294002, a PI3K inhibitor, attenuated the anti-apoptotic effect of salidroside and blocked the increase of Akt and mTOR; however, did not affect the antioxidative effect of salidroside. These findings suggested that salidroside was capable of protecting HUVECs against H2O2-induced apoptosis by activating the PI3K/Akt/mTOR-dependent pathway and inhibiting ROS production by activating REDD1.

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