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Background We aimed to explore the relationship between the neutrophil to lymphocyte ratio (NLR) and the early clinical outcomes in children with congenital heart disease (CHD) associated with pulmonary arterial hypertension (PAH) after cardiac surgery. Methods A retrospective observational study involving 190 children from January 2013 to August 2019 was conducted. Perioperative clinical and biochemical data were collected. Results We found that pre-operative NLR was significantly correlated with AST, STB, CR and UA (P < 0.05), while post-operative NLR was significantly correlated with ALT, AST, BUN (P < 0.05). Increased post-operative neutrophil count and NLR as well as decreased lymphocyte count could be observed after cardiac surgery (P < 0.05). Level of pre-operative NLR was significantly correlated with mechanical ventilation time, ICU stay time and total length of stay (P < 0.05), while level of post-operative NLR was only significantly correlated to the first two (P < 0.05). By using ROC curve analysis, relevant areas under the curve for predicting prolonged mechanical ventilation time beyond 24 h, 48 h and 72 h by NLR were statistically significant (P < 0.05). Conclusion For patients with CHD-PAH, NLR was closely related to early post-operative complications and clinical outcomes, and could act as a novel marker to predict the occurrence of prolonged mechanical ventilation.

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The expression of microRNA-802 (miR-802) is known to be associated with insulin resistance (IR); however, the mechanism remains unclear. The present study investigated how miR-802 contributes to the development of IR using C57BL/6J mice fed a high-fat diet (HFD) to establish a model of IR. Adeno-associated virus overexpressing miR-802 was administered to the mice via tail vein injection. The effects of miR-802 on reactive oxygen species (ROS), lipid peroxidation (LPO) and the activities of multiple ROS-related enzymes were investigated. Western blot analysis was used to estimate the protein levels of extracellular signal regulated kinase (ERK), p38mitogen-activated protein kinases (p38MAPK), c-Jun N-terminal kinase (JNK), insulin receptor substrate 1 (IRS-1) and protein kinase B (AKT1). The results demonstrated that the levels of ROS and LPO production were increased in the livers of the miR-802-treated group compared with the control group. The activities of the ROS-related enzymes were reduced. Furthermore, the expression of phosphorylated (phosphor)-p38MAPK and phosphor-JNK were upregulated in the miR-802 overexpression group, whereas there was no difference in the expression levels of phosphor-ERK. The expression levels of phosphor-AKT1 were reduced in the miR-802-treated group and these effects were reversed by miR-802 knockdown. In conclusion, the results demonstrate that miR-802 may cause IR by activating the JNK and p38MAPK pathways to increase hepatic oxidative stress.

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