Neural stem cell (NSC) transplantation has prevailed as a promising protective strategy for cardiac arrest (CA)-induced brain damage. Surprisingly, the poor survival of neuronal cells in severe hypoxic condition restricts the utilization of this cell-based therapy. Extracellular vesicles (EVs) transfer microRNAs (miRNAs) between cells are validated as the mode for the release of several therapeutic molecules. The current study reports that the bone marrow mesenchymal stem cells (BMSCs) interact with NSCs via EVs thereby affecting the survival of neuronal cells. Hypoxic injury models of neuronal cells were established using cobalt chloride, followed by co-culture with BMSCs and NSCs alone or in combination. BMSCs combined with NSCs elicited as a superior protocol to stimulate neuronal cell survival. BMSCs-derived EVs could protect neuronal cells against hypoxic injury. Silencing of miR-133b incorporated in BMSCs-derived EVs could decrease the cell viability and the number of NeuN-positive cells and increase the apoptosis in the CA rat model. BMSCs-derived EVs could transfer miR-133b to neuronal cells to activate the AKT-GSK-3β-WNT-3 signaling pathway by targeting JAK1. Our study demonstrates that NSCs promotes the release of miR-133b from BMSCs-derived EVs to promote neuronal cell survival, representing a potential therapeutic strategy for the treatment of CA-induced brain damage.

rhGH does not accelerate the proli-feration of human gastric cancer cell in vivo.

neural stem cells (nScs) have the potential to give rise to offspring cells and hypoxic injury can impair the function of nScs. The present study investigated the effects of mesenchymal stem cell (MSc)-derived extracellular vesicles (eVs) on nSc injury, as well as the underlying mechanisms. MSC-EVs were isolated and identified via morphological and particle size analysis. cobalt chloride was used to establish a hypoxic injury model in nScs. Terminal deoxynucleotidyl transferase duTP nick end labeling assay was conducted to detect apoptosis. reverse transcription-quantitative Pcr was performed to detect the expression levels of mir-210-3p, and western blotting was used to detect the expression levels of apoptosis-inducing factor (aiF) and Bcl-2 19 kda interacting protein (BniP3). compared with the control group, nSc apoptosis, and the expression of mir-210-3p, aiF and BniP3 were significantly higher in the cobalt chloride-induced hypoxia group. By contrast, treatment with MSc-eVs further increased mir-210-3p expression levels, but reduced nSc apoptosis and the expression levels of aiF and BniP3 compared with the model group (P<0.05). in addition, mir-210-3p inhibitor reduced mir-210-3p expression, but promoted hypoxia-induced apoptosis and the expression levels of aiF and BniP3 compared with the model group (P<0.05). collectively, the results suggested that MSc-eVs prevented nSc hypoxia injury by promoting mir-210-3p expression, which might reduce aiF and BniP3 expression levels and nSc apoptosis.

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Background The success rate of rescue is extremely low in acute paraquat poisoning. This study aimed to assess whether strengthened hemoperfusion (SHP) combined with continuous venovenous hemofiltration (CVVH) improves prognosis in patients with acute paraquat poisoning. Methods Patients from January 2005 to December 2018 were enrolled retrospectively. All selected patients were administered conventional therapy. They were divided according to the received treatments in the conventional therapy, hemoperfusion (HP), CVVH, SHP and SHP + CVVH groups. Follow-up was implemented until the 90th day after poisoning. Other outcomes included all-cause mortality on the 15th day after poisoning, and the percentages of respiratory failure and mechanical ventilation use. Results The study included 487 patients,and 211 died in all. Mortality rate in the SHP + CVVH group on the 90th day after poisoning was significantly decreased compared with those of other groups (p<0.001). Survival curves of all groups showed significant differences (p<0.001). SHP combined with CVVH was an independent factor reducing mortality risk (p<0.001). Mortality rate in the SHP + CVVH group on the 15th day after poisoning was also significantly decreased (p < 0.05). The proportions of patients in the SHP + CVVH group with acute respiratory failure and mechanical ventilation were significantly lower than those of other groups (p < 0.05). Conclusions SHP with CVVH may decrease the mortality rate of patients with acute paraquat poisoning on the 90th day after poisoning and improve the prognosis.