RESUMO
OBJECTIVE: The growth and migration of airway smooth muscle cells (ASMCs) are dysregulated in asthma. MicroRNAs (miRNAs) are associated with the pathogenesis of many diseases including asthma. Instead, the function of miR-140- 3pin ASMCs' dysregulation in asthma remains inconclusive. This study aimed to explore the role and mechanism of miR-140-3p in ASMCs' dysregulation. MATERIALS AND METHODS: In this experimental study, ASMCs were stimulated with platelet-derived growth factor (PDGF)- BB to construct an asthma cell model in vitro. MiR-140-3p expression level in the plasma of 50 asthmatic patients and 50 healthy volunteers was measured with quantitative real-time polymerase chain reaction (qRT-PCR). Besides, the enzyme-linked immunosorbent assay (ELISA) was applied to detect the contents of interleukin (IL) -1ß, IL-6, and tumor necrosis factor-α (TNF-α) in the cell culture supernatant of ASMCs. Additionally, CCK-8 and transwell assays were adopted to probe the multiplication and migration of ASMCs. In addition, the western blot was employed to examine HMGB1, JAK2, and STAT3 protein expressions in ASMCs after miR-140-3p and HMGB1 were selectively regulated. RESULTS: miR-140-3p expression was declined in asthmatic patients' plasma and ASMCs stimulated by PDGF-BB. Upregulating miR-140-3p suppressed the viability and migration of the cells and alleviated the inflammatory response while inhibiting miR-140-3p showed opposite effects. Additionally, HMGB1 was testified as the target of miR-140-3p. HMGB1 overexpression could reverse the impact of miR-140-3p upregulation on the inflammatory response of ASMCs stimulated by PDGF-BB. MiR-140-3p could repress the activation of JAK2/STAT3 via suppressing HMGB1. CONCLUSION: In ASMCs, miR-140-3p can inhibit the JAK2/STAT3 signaling pathway by targeting HMGB1, thus ameliorating airway inflammation and remodeling in the pathogenesis of asthma.
RESUMO
BACKGROUND The aim of this study was to analyze amplitude-integrated electroencephalography (aEEG) in early diagnosis and prognosis of hypoxic encephalopathy (HE) in premature infants. MATERIAL AND METHODS Thirty-six premature infants with HE who were treated in Linyi Central Hospital were enrolled into the study group, while 40 premature infants without HE were assigned into the control group. aEEG was conducted within 6 h after delivery to compare aEEG continuity, mature sleep-wake cycle, and maximum and minimum voltage in the 2 groups. Correlations between aEEG abnormalities and clinical grading, neurological prognosis, Apgar score, and blood gas were also analyzed among the premature infants with HE. RESULTS Compared with the control group, there were reductions in the continuous rate of aEEG, mature sleep-wake cycle, and the minimum voltage, and an increase in the maximum voltage in the study group (all P<0.05). The study group had a higher abnormal rate of aEEG and a lower normal rate of aEEG than in the control group (both P<0.05). Spearman's rank correlation coefficients for abnormal aEEG and clinical grade and poor neurological prognosis were 0.758 and 0.799, respectively. The sensitivity of abnormal aEEG in predicting severity of clinical grading was 100% with a specificity of 82.5%. The sensitivity of abnormal aEEG in predicting neurological prognosis was 100% with a specificity of 90.3%. The Apgar scores and blood glass pH of the infants with various abnormal rates of aEEG were significantly different at 1 min, 5 min, and 10 min after delivery (all P<0.05). CONCLUSIONS HE in premature infants has specific aEEG characteristics, which can be used to predict the severity and prognosis of HE.
