LncRNA SNHG12 suppresses adipocyte inflammation and insulin resistance by regulating the HDAC9/Nrf2 axis.

Obesity is often associated with low-grade inflammation. The incidence of obesity has increased annually worldwide, which seriously affects human health. A previous study indicated that long noncoding RNA SNHG12 was downregulated in obesity.

Postnatal feeding with high-fat combined with high-glucose diet induces precocious puberty in Sprague‒Dawley rat pups.

With economic development and overnutrition, including high-fat diets (HFD) and high-glucose diets (HGD), the incidence of obesity in children is increasing, and thus, the incidence of precocious puberty is increasing. Therefore, it is of great importance to construct a suitable animal model of overnutrition-induced precocious puberty for further in-depth study. Here, we fed a HFD, HGD, or HFD combined with a HGD to pups after P-21 weaning, while weaned pups fed a normal diet served as the control group.

TFAP2C inhibits cell autophagy to alleviate myocardial ischemia/reperfusion injury by regulating miR-23a-5p/SFRP5/Wnt5a axis.

Myocardial ischemia/reperfusion (MI/R) injury contributes to severe injury for cardiomyocytes. In this study, we aimed to explore the underlying mechanism of TFAP2C on cell autophagy in MI/R injury. MTT assay measured cell viability.

Gut microbiome combined with metabolomics reveals biomarkers and pathways in central precocious puberty.

Background: Central precocious puberty (CPP) is a common disease in prepubertal children and results mainly from disorders in the endocrine system. Emerging evidence has highlighted the involvement of gut microbes in hormone secretion, but their roles and downstream metabolic pathways in CPP remain unknown.

Methods: To explore the gut microbes and metabolism alterations in CPP, we performed the 16S rRNA sequencing and untargeted metabolomics profiling for 91 CPP patients and 59 healthy controls.

Exosomal miR-122 promotes adipogenesis and aggravates obesity through the VDR/SREBF1 axis.

Objective: This study examined the effects of miR-122-enriched exosomes on the expression of vitamin D3 receptor (VDR) and sterol regulatory element-binding transcription factor 1 (SREBF1) and their roles during adipogenesis.

Methods: The roles of miR-122, SREBF1, and VDR were investigated during adipogenesis. The relationships between VDR and miR-122 or SREBF1 were assessed by dual-luciferase reporter and chromatin immunoprecipitation assays.

EGCG protects against myocardial I/RI by regulating lncRNA Gm4419-mediated epigenetic silencing of the DUSP5/ERK1/2 axis.

Background: Epigallocatechin gallate (EGCG) has attracted increasing attention due to its beneficial effect on cardiovascular health. The aim of this study was to investigate the underlying mechanism by which EGCG protects against myocardial ischaemia/reperfusion injury (I/RI).

Methods: Murine myocardial I/RI and HO-induced cardiomyocyte injury models were established to evaluate the therapeutic effects of EGCG.

Effects and mechanism of arachidonic acid against TNF-α induced apoptosis of endothelial cells.

This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry.

Reactive oxygen species contribute to simulated ischemia/reperfusion-induced autophagic cell death in human umbilical vein endothelial cells.

Background: Autophagy is important for cells to degrade protein aggregates and organelles. Our preliminary study suggests that ischemia/reperfusion in rabbit hearts promoted autophagic myocardial injury, resulting in no-reflow phenomenon. In this study, we sought to further understand the mechanism and outcome of the upregulation of autophagy in ischemia/reperfusion.

NF-κB-mediated induction of autophagy in cardiac ischemia/reperfusion injury.

Ischemia/reperfusion (I/R) injury severely attenuates the benefit of revascularization after acute myocardial infarction, in which transcription factor NF-κB plays an important role. Recently, there is increasing evidence to suggest that autophagy is involved in this process. We sought to define the role of NF-κB in the induction of autophagy during cardiac I/R injury.

Cytochrome P-450 epoxygenases protect endothelial cells from apoptosis induced by tumor necrosis factor-alpha via MAPK and PI3K/Akt signaling pathways.

Endothelial cells play a vital role in the maintenance of cardiovascular homeostasis. Epoxyeicosatrienoic acids (EETs), cytochrome P-450 (CYP) epoxygenase metabolites of arachidonic acid in endothelial cells, possess potent and diverse biological effects within the vasculature. We evaluated the effects of overexpression of CYP epoxygenases on tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis in bovine aortic endothelial cells.

Cytochrome P450 2J2 promotes the neoplastic phenotype of carcinoma cells and is up-regulated in human tumors.

Cytochrome P450 (CYP) arachidonic acid epoxygenase 2J2 converts arachidonic acid to four regioisomeric epoxyeicosatrienoic acids, which exert diverse biological activities in cardiovascular system and endothelial cells. However, it is unknown whether this enzyme highly expresses and plays any role in cancer. In this study, we found that very strong and selective CYP2J2 expression was detected in human carcinoma tissues in 101 of 130 patients (77%) as well as eight human carcinoma cell lines but undetectable in adjacent normal tissues and nontumoric human cell lines by Western, reverse transcription-PCR, and immunohistochemical staining.