Effect of Yangxin Huoxue Jiedu recipe on inflammatory factors and oxidative stress on viral myocarditis in children.

OBJECTIVE: This observation purposed to investigate the effect of the Yangxin Huoxue Jiedu formula on children with viral myocarditis and its effect on inflammatory factors and oxidative response. MATERIALS AND METHODS: A total of 121 children with viral myocarditis were randomly divided into two groups, namely the control group (N = 60) and the traditional Chinese medicine group (N = 61). The control group was mainly treated with routine therapy, while the traditional Chinese medicine group was treated with Yangxin Huoxue Jiedu recipes based on the control group. The creatine kinase, creatine kinase myocardial isoenzyme, aspartate aminotransferase, lactic dehydrogenase, hydroxybutyrate dehydrogenase, cardiac troponin I, brain natriuretic peptide, interleukin-6, interleukin-8, and tumour necrosis factor-alpha, superoxide dismutase and malondialdehyde in viral myocarditis patients were tested to estimate the myocardial function, inflammation, and oxidative situation. RESULTS: After Yangxin Huoxue Jiedu treatment, 15 cases were recovered, 20 were excellent, and 21 were effective, which had a significant difference from the control group. The concentration of creatine kinase, creatine kinase myocardial isoenzyme, aspartate aminotransferase, lactic dehydrogenase, hydroxybutyrate dehydrogenase, cardiac troponin I and brain natriuretic peptide was decreased in the traditional Chinese medicine group. The levels of interleukin-6, interleukin-8, and tumour necrosis factor-alpha in the traditional Chinese medicine group were significantly lower than those in the control group. Superoxide dismutase was higher and malondialdehyde was lower than those in the control group. CONCLUSION: The use of Yangxin Huoxue Jiedu in the treatment of viral myocarditis has a definite clinical effect, which could improve myocardial function, reduce body inflammation, and promote oxidative recovery.

MiR-338-3p Is a Biomarker in Neonatal Acute Respiratory Distress Syndrome (ARDS) and Has Roles in the Inflammatory Response of ARDS Cell Models.

To investigate the association between serum miR-338-3p levels and neonatal acute respiratory distress syndrome (ARDS) and its mechanism. The relative miR-338-3p expression in serum was detected by quantitative real-time RT-PCR. Interleukin-1beta (IL-1ß), IL-6, and tumor necrosis factor-alpha (TNF-α) levels were detected by ELISAs. A receiver operating characteristic (ROC) curve analysis of serum miR-338-3p evaluated the diagnosis of miR-338-3p in neonatal ARDS. Pearson's correlation analysis evaluated the correlation between serum miR-338-3p and neonatal ARDS clinical factors. Flow cytometry evaluated apoptosis, and a CCK-8 assay assessed cell viability. A luciferase assay evaluated the miR-338-3p/AKT3 relationship. The miR- 338-3p expression was decreased in neonatal ARDS patients and in lipopolysaccharide (LPS)-treated cells. The ROC curve showed the accuracy of miR-338-3p for evaluating neonatal ARDS patients. The correlation analysis demonstrated that miR-338-3p was related to PRISM-III, PaO2/FiO2, oxygenation index, IL-1ß, IL-6, and TNF-α in neonatal ARDS patients. MiR-338-3p overexpression inhibited the secretion of inflammatory components, stifled cell apoptosis, and LPS-induced advanced cell viability. The double-luciferase reporter gene experiment confirmed that miR-338-3p negatively regulates AKT3 mRNA expression. Serum miR-338-3p levels were related to the diagnosis and severity of neonatal ARDS, which may be attributed to its regulatory effect on inflammatory response in ARDS.

MiR-629-5p May serve as a biomarker for pediatric acute respiratory distress syndrome and can regulate the inflammatory response.

OBJECTIVE: Circulating microRNAs (miRNAs) are associated with pediatric acute respiratory distress syndromes (PARDS). This study analyzed the clinical significance and potential mechanism of microRNA (miR)-629-5p in PARDS. METHODS: 82 children with PARDS and 82 controls were enrolled. Serum levels of miR-629-5p were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its diagnostic significance with respect to for PARDS in children was assessed by the receiver operating characteristic (ROC). Kaplan-Meier curve and multivariate Cox regression were utilized to examine the prognostic significance of miR-629-5p. An in vitro cell model was established using lipopolysaccharide (LPS)-induced alveolar epithelial cells A549. The cell proliferation, apoptosis, and inflammatory factors were assessed using cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA). miR-629-5p target genes were identified in the database and validated using the dual-luciferase report assay. RESULTS: Serum miR-629-5p levels were significantly higher in children with PARDS than in controls (P < 0.05). miR-629-5p exhibited 86.6% sensitivity and 91.5% specificity in distinguishing children with PARDS. miR-629-5p was an independent risk factor for mortality, and high levels of miR-629-5p have a poor prognosis. LPS promoted apoptosis and overproduction of inflammatory factors in A549 and upregulated miR-629-5p expression (P < 0.05); however, they were partially reversed by the weakened miR-629-5p (P < 0.05). Syndecan-4 (SDC4) is a target of miR-629-5p. The inhibition of SDC4 induced by LPS can be alleviated through the reduction of miR-629-5p. CONCLUSION: miR-629-5p serves as a diagnostic biomarker for children with PARDS and it is associated with poor prognosis. Diminished miR-629-5p may alleviate PARDS by targeting SDC4 to suppress apoptosis and inflammation of alveolar epithelial cells.

[Le miR-224-5p régulé sert de biomarqueur pour l'insuffisance hépatique aiguë pédiatrique et régule l'inflammation en modulant ZBTB20]. / Upregulated miR-224-5p served as a biomarker for pediatric acute liver failure and regulate inflammation by modulating ZBTB20.

Pediatric acute liver failure (PALF) is a severe liver dysfunction with complex pathological mechanisms and rapid development. MiRNAs have been identified as promising biomarkers for human disease screening and monitoring. This study focused on evaluating the clinical significance of miR-224-5p in PALF and revealing its potential molecular mechanism in regulating liver cell injury. This study enrolled 103 children with PALF and 55 healthy children without liver diseases. Serum miR-224-5p levels were compared between the two groups, and their clinical significance was estimated by analyzing the correlation with clinicopathological features and outcomes of PALF children. In vitro, a normal liver cell was treated with lipopolysaccharide (LPS), and cell growth and inflammation were assessed by CCK8 and ELISA assay. Upregulated miR-224-5p in PALF showed significance in screening PALF children from healthy children with the sensitivity and specificity of 78.64% and 84.47%, respectively. Increasing serum miR-224-5p in PALF children was closely associated with increasing prothrombin time, alanine transaminase, international normalized ratio, total bilirubin, ammonia, and aspartic transaminase and decreasing albumin of PALF children. MiR-224-5p was also identified as a risk factor for adverse outcomes in children with PALF. In LPS-treated liver cells, miR-224-5p could negatively regulate ZBTB20, and silencing miR-224-5p could alleviate the inhibited cell growth and promoted inflammation by LPS, which was reversed by ZBTB20 knockdown. Increasing miR-224-5p distinguished PALF children, predict severe disease development and risk of adverse prognosis. miR-224-5p also reguled LPS-induced liver cell injury via negatively regulating ZBTB20.