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The overexpression of LINC00511 significantly elevated the viability and EdU-positive rate in H2O2-treated cardiomyocytes. LINC00511 could bind to miRNA-515-5p. Meanwhile, there was a negative correlation between the levels of LINC00511 and miRNA-515-5p. In addition, the overexpression of miRNA-515-5p reversed the promoting effect of LINC00511 on the proliferative ability of H2O2-treated cardiomyocytes. CONCLUSIONS LINC00511 accelerates the proliferation of cardiomyocytes after I/R by targeting miRNA-515-5p.OBJECTIVE The aim of this study was to explore the influence of hydrogen sulfide (H2S) on cardiomyocyte apoptosis in rats with myocardial ischemia-reperfusion injury via the c-Jun N-terminal kinase (JNK) pathway. find more MATERIALS AND METHODS A total of 60 normal female Sprague-Dawley (SD) rats aged 38 weeks were divided into 3 groups, including the sham operation group (n=20), ischemia group (n=20) and ischemia + sodium hydrosulfide (NaHS) group (n=20). Subsequently, differences in cardiac function, the morphology of myocardial tissues, protein expression of JNK2, the content of plasma H2S and malondialdehyde (MDA), the activity of superoxide dismutase (SOD), cystathionine-γ-lyase (CSE) and glutathione peroxidase (GSH-Px) were analyzed among rats in all groups. RESULTS Left ventricular diastolic pressure (LVDP) and maximum rate of pressure rise/fall (± dP/dtmax) were the highest in of rats of the sham operation group and the lowest in the ischemia group. Meanwhile, they were significantly elevated in the ischemia + tein expression level of phosphorylated JNK2, with the highest level in the ischemia group. The content of MDA in rat myocardial tissues was markedly higher in the ischemia group than that of the ischemia + NaHS group, with the lowest level in the sham operation group (p less then 0.01). Additionally, the activity of SOD and GSH-Px in rat myocardial tissues was remarkably worse in the ischemia group than that of the ischemia + NaHS group, and it was the strongest in the sham operation group (p less then 0.01). CONCLUSIONS H2S inhibits the activity of the JNK pathway, decreases its phosphorylation level and down-regulates the protein expression level of JNK2, thereby protecting against myocardial ischemia-reperfusion injury.OBJECTIVE Obstructive Sleep Apnea Syndrome (OSAS) is a disorder characterized by recurrent upper airway obstruction, apnea, and hypopnea, associated with decreased oxygen saturation and disturbed sleep structure during sleep. It was found that OSAS was associated with a variety of arrhythmia and conduction disorders, but the relationship between multiple types of arrhythmia and the severity of OSAS, and its possible mechanism remain unclear. The purpose of this study was to observe the main types of arrhythmia and the condition of heart rate variability (HRV) in patients with OSAS, to detect the levels of multiple inflammatory factors in serum of OSAS patients, and to observe the correlation between polysomnographic parameters or inflammatory factors, and arrhythmia or HRV, as well as its possible mechanisms. PATIENTS AND METHODS 141 patients with suspected OSAS were collected in the Second Affiliated Hospital of Soochow University and Xinghua People's Hospital from February 2016 to February 2018. According to the sleep apnea hypopnea index (AHI), they were divided into control group (AHI 0.05). There was a significant positive correlation between hs-CRP and oxygen reduction index (ODI) (r=0.209, p=0.013) and a significant negative correlation with PNN50 (r=-0.188, p=0.025). There is no significant correlation between other indicators. CONCLUSIONS Systemic inflammatory reactions existed in patients with OSAS. With the increase of OSAS, inflammation was aggravated, especially serum hs-CRP. Hs-CRP was significantly and negatively correlated with PNN50 and positively correlated with ODI. The results suggested that the inflammatory response was involved in the occurrence of heart rate variability in OSAS patients.OBJECTIVE To explore the role of imatinib in desoxycorticosterone acetate (DOCA)-induced myocardial fibrosis in rats by the p38 mitogen-activated protein kinase (MAPK) signaling pathway. MATERIALS AND METHODS Normal group (n=20), DOCA induction group (n=20), and imatinib treatment group (treatment group, n=20) were set up. Then, the cardiac function was examined via magnetic resonance imaging (MRI) and echocardiography (ECG) on the 21st d after modeling. Alkaline phosphatase (ALP) and myocardial function index creatine kinase-MB (CK-MB) were detected. The enzyme-linked immunosorbent assay (ELISA) was performed to measure tumor necrosis factor-gamma (TNF-γ) and interleukin-6 (IL-6). Hematoxylin-eosin (HE) staining assay was carried out to observe the pathological changes in myocardial tissues. Quantitative Polymerase Chain Reaction (qPCR) and Western blotting were employed to measure the expression levels of important myocardial fibrosis-related genes [checkpoint kinase 1 (Chek1) and alpha-smooth muscle actin egulate the repair of myocardial injury caused by DOCA-induced myocardial fibrosis in rats by repressing the p38 MAPK signaling pathway.OBJECTIVE To explore the effect of the micro ribonucleic acid (miR)-223 on the thrombophlebitis rats by regulating the Toll-like receptor (TLR) signaling pathway. MATERIALS AND METHODS The rat model of thrombophlebitis was established, and miR-223 was silenced or overexpressed through lentiviral transfection. The rats were divided into miR-223 inhibitors group (Inhibitors group), miR-223 mimics group (Mimics group), and normal group (Control group). The transfection efficiency of miR-223 in venous tissues was detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR), the hemorheological indexes plasma viscosity (PV) and hematocrit (HCT) were observed, and the content of the serum inflammatory factors interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the fibrinolytic indexes plasminogen activator inhibitor (PAI) and the tissue-type plasminogen activator (t-PA) were detected, the morphological changes in the venous tissues were observed via hematoxylin-eosin (HE) staining, and the gene and protein expressions of the TLR signaling pathway were detected via RT-PCR and Western blotting.