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1.
Oxid Med Cell Longev ; 2022: 1030238, 2022.
Article in English | MEDLINE | ID: covidwho-2194204

ABSTRACT

The effective remission of acute respiratory distress syndrome- (ARDS-) caused pulmonary fibrosis determines the recovery of lung function. Inositol can relieve lung injuries induced by ARDS. However, the mechanism of myo-inositol in the development of ARDS is unclear, which limits its use in the clinic. We explored the role and mechanism of myo-inositol in the development of ARDS by using an in vitro lipopolysaccharide- (LPS-) established alveolar epithelial cell inflammation model and an in vivo ARDS mouse model. Our results showed that inositol can alleviate the progression of pulmonary fibrosis. More significantly, we found that inositol can induce autophagy to inhibit the progression pulmonary fibrosis caused by ARDS. In order to explore the core regulators of ARDS affected by inositol, mRNA-seq sequencing was performed. Those results showed that transcription factor HIF-1α can regulate the expression of SLUG, which in turn can regulate the key gene E-Cadherin involved in cell epithelial-mesenchymal transition (EMT) as well as N-cadherin expression, and both were regulated by inositol. Our results suggest that inositol activates autophagy to inhibit EMT progression induced by the HIF-1α/SLUG signaling pathway in ARDS, and thereby alleviates pulmonary fibrosis.


Subject(s)
Pulmonary Fibrosis , Respiratory Distress Syndrome , Mice , Animals , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/chemically induced , Inositol/adverse effects , Signal Transduction , Respiratory Distress Syndrome/drug therapy , Cadherins/metabolism , Autophagy , Epithelial-Mesenchymal Transition , Lipopolysaccharides/pharmacology
2.
Risk Manag Healthc Policy ; 13: 2669-2675, 2020.
Article in English | MEDLINE | ID: covidwho-948008

ABSTRACT

PURPOSE: Pandemic-related confinement helps to contain the transmission of the novel coronavirus disease (COVID-19) but restricts children's exposure to sunlight, thereby possibly affecting their 25-hydroxyvitamin D [25(OH)D] levels. This study aimed to examine the effect of COVID-19 measures on 25(OH)D levels in children. PATIENTS AND METHODS: This study included children who underwent health checks between March 1 and June 30, 2020, and those over the equivalent period during 2017-2019 (N = 3600). Children's 25(OH)D levels and the proportion of children with vitamin D deficiency were compared between different observation periods. RESULTS: The mean serum 25(OH)D level was 84 ± 25nmol/L. The overall proportion of children with vitamin D deficiency (25(OH)D level <50 nmol/L) was 4.6%. Home confinement led to an increase in the proportion of children aged 3-6 years with vitamin D deficiency during March 1-June 30, 2020 compared with the same months in previous years, and the most noticeable increase was found in March 2020. In children aged 3-6 years, 25(OH)D levels were lower in 2020 (65 ± 17nmol/L) than during 2017-2019, and the proportion of those with vitamin D deficiency was higher in 2020 (19.0%) than in previous years. Among children aged 0.5-1 and 1-3 years, 25(OH)D levels were higher (97 ± 25 nmol/L, 91 ± 27 nmol/L), while the proportion of children with vitamin D deficiency was lower in 2020 (2.3%, 3.0%) than during 2017-2019. CONCLUSION: The 25(OH)D levels tended to decrease gradually with increasing age. Reduced sunlight exposure during confinement is associated with lower 25(OH)D levels among children aged 3-6 years. Therefore, vitamin D supplementation for children aged >3 years is recommended.

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