BackgroundH2S can also protect nerve cells. The objective of the study is to investigate the effects of hydrogen sulfide (H2S) on the expressions of brain-derived neurotrophic factor (BDNF) and its receptors, tyrosine protein kinase B (TrkB) and p75 neurotrophin receptor (p75NTR), in brain tissues of rats with cardiac arrest and cardiopulmonary resuscitation (CA/CPR) following the restoration of spontaneous circulation (ROSC).MethodsRats (n = 240) with CA/CPR were divided into three groups: Intervention (n = 80) that received sodium hydrosulfide (NaHS, 14 μmoL/kg·d) intervention after ROSC; Inhibition (n = 80) that received hydroxylamine (40 μmoL/kg·d) intervention after ROSC; and Control (n = 80) that received saline after ROSC. Kaplan-Meyer analysis was used to analyze the survival data. Quantitative real-time PCR (q-PCR), Western blot, immunohistochemistry and IODs (integrated optical density) were performed to determine the mRNA and protein expressions of BDNF, TrkB and p75NTR in rat brain tissues.ResultsSurvival rate of the three groups had significant difference (χ2 = 28.376, p = 0.000). The Intervention group had the highest survival rate (82.5%), while the Inhibition group had the lowest survival rate (62.5%). The mRNA and protein levels of BDNF and TrkB in the Intervention group were significantly higher compared to the Control group (p < 0.05); while the mRNA and protein levels of BDNF and TrkB in the Inhibition group was significantly lower than the Control group (p < 0.05) on days 1, 3, and 7. However, the mRNA and protein levels of p75NTR in the Intervention group were significantly lower than the Control group (p < 0.05); while the mRNA and protein levels of p75NTR in the Inhibition group were significantly higher than the Control group (p < 0.05) on days 1, 3, and 7.ConclusionNaHS treatment increases the survival rate of rats after CA and ROSC by upregulating the expression and activation of BDNF and its receptor TrkB, and down-regulating p75NTR expression.

Background: Cardiac arrest (CA), a common disease with a high mortality rate, is a leading cause of ischemia/reperfusion (I/R)-induced dysfunction of the intestinal barrier. Long non-coding RNAs (lncRNAs) play crucial roles in multiple pathological processes. However, the effect of the lncRNA maternally expressed 3 (MEG3) on intestinal I/R injury and the intestinal barrier has not been fully determined. Therefore, this study aimed to investigate the function of MEG3 in CA-induced intestinal barrier dysfunction. Methods:The oxygen and glucose deprivation (OGD) model in the human colorectal adenocarcinoma Caco-2 cells and in vivo cardiac arrest-induced intestinal barrier dysfunction model in Sprague-Dawley (SD) rats were established. The effect and underlying mechanism of MEG3 on the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury were analyzed by methyl thiazolyl tetrazolium (MTT) assays, Annexin V-FITC/PI apoptosis detection kit, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, quantitative polymerase chain reaction (qPCR) assays, Western blot analysis, luciferase reporter gene assays, transepithelial electrical resistance (TEER) measurements, immunofluorescence analysis, and enzyme-linked immunosorbent assay (ELISA) assays.Results: Interestingly, we found that MEG3 could protect Caco-2 cells from oxygen-glucose deprivation (OGD)/reoxygenation-induced I/R injury by modulating cell proliferation and apoptosis. Moreover, MEG3 relieved OGD-induced intestinal barrier dysfunction in vitro, as demonstrated by its significant rescue effect on transepithelial electrical resistance and the expression of tight junction proteins such as occludin and claudin-1 (CLDN1), which were impaired in OGD-treated Caco-2 cells. Mechanistically, MEG3 inhibited the expression of inflammatory factors including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, interferon-gamma (IFN)-γ, inflammatory factors including interleukin (IL)-10, and transforming growth factor beta (TGFb)-1, as well as nuclear factor-kappa B (NF-κB) signaling. In response to OGD treatment in vitro, MEG3 also activated the expression of sirtuin 1 (SIRT1) by Caco-2 cells via sponging miR-34a-3p. Furthermore, MEG3 relieved CA-induced intestinal barrier dysfunction through NF-κB signaling in vivo.Conclusions: LncRNA MEG3 can protect the intestinal barrier from cardiac arrest-induced I/R injury via miR-34a-3p/SIRT1/NF-κB signaling. This finding provides new insight into the mechanism by which MEG3 restores intestinal barrier function following I/R injury, presenting it as a potential therapeutic candidate or strategy in intestinal injury.