Objective: To understand the mental health status and its risk factors among discharged COVID-19 patients during the first month of centralized quarantine and the subsequent home isolation.Methods: The scales of the Insomnia Severity Index (ISI), General Anxiety Disorder (GAD-7), and Patient Health Questionnaire (PHQ-9) were used to measure the symptoms of insomnia, anxiety, and depression in 782 COVID-19 patients during the first month of centralized quarantine (March 16 to 26, 2020) and then during home isolation (April 3 to 10, 2020).Results: During the centralized quarantine, the prevalence rates of insomnia, anxiety, and depressive symptoms were 44.37, 31.59, and 27.62%, respectively, and those during the home isolation decreased significantly at 27.11, 17.26, and 16.11%, respectively. In both waves, women showed a higher prevalence of symptoms of poor mental health compared to men, and middle-aged (40–59 years old) and elderly (≥60 years old) showed a higher risk of symptoms of poor mental health compared to the younger. In addition, the severity of COVID-19 revealed no significant relationship to symptoms of poor mental health, whereas, the interaction analysis revealed that those with other underlying diseases showed more symptoms of poor mental health during the centralized quarantine and a greater decrease during the follow-up home isolation.Conclusion: The discharged COVID-19 patients suffered from mental health problems such as, insomnia, depression, and anxiety, and this was especially so for women, the middle-aged and elderly, and those with underlying diseases, but along with the rehabilitation and the environmental change from centralized quarantine to home isolation, all the mental symptoms were significantly alleviated. Based on a follow-up investigation, the current results provide critical evidence for mental health and early rehabilitation upon the discharged COVID-19 patients.
Objective. Microglial BV-2 cells are activated in the brain following insomnia. Naringin (NAR) is a polymethoxylated flavonoid that is also commonly found in citrus fruits and is known for its antioxidant potential. However, the effect of NAR on microglial cells has rarely been studied in the brain of an organism after insomnia. This study aimed to investigate the effects and potential mechanisms of action of NAR on microglial cell activation and inflammation. Methods. BV-2 cells were obtained from the China Center for Type Culture Collection and randomly divided into five treatment groups: control, model, NAR (10 μM), WP1066 (5 μM), and NAR + WP1066. With the exception of the control group, all groups were stimulated with LPS (1 μg/mL) for 6 h. CCK8 was used to quantify cell viability and a scratch test was performed to detect cell migration. The expression levels of interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), nterleukin 10 (IL-10), and insulin like growth factor (1IGF-1) were measured by ELISA. Western blotting was performed to determine the levels of p-STAT3 and p-JAK. The Focalcheck™ Thin-Ring Fluorescent Microspheres kit was used to detect cell phagocytosis. Immunofluorescence was used to observe the expression of iNOS and arginase1 in BV-2 cells. Results. Compared with the control group, cell migration, cell viability, and the expression of IL-1β, IL-6, TNF-α, and iNOS were significantly increased in the model group, whereas the expression levels of IL-10, IGF-1, and arginase 1, as well as cell phagocytosis were reduced. With the increase in NAR concentration, cell migration, cell viability, the expression levels of IL-1β, IL-6, TNF-α, and iNOS decreased, while the expression of IL-10, IGF-1, and arginase 1 increased. Compared with the control group, p-STAT3, and p-JAK expression in the model group were significantly increased (P<0.05). Compared with the model group, the expression of p-STAT3 and p-JAK in the NAR, NAR + WP1066, and WP1066 groups was significantly decreased ( P < 0.05 ). Conclusion. NAR treatment inhibited the proliferation, migration, and inflammation of BV-2 cells as well as the activation of microglia to the M1 phenotype. Conversely, NAR treatment promoted the activation of microglia to the M2 phenotype and enhanced the phagocytic function of BV-2 cells by regulating the activity of the JAK/STAT3 pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.