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Background: Intestinal ischemia/reperfusion (I/R) injury is a severe condition associated with high morbidity and mortality. Ischemic preconditioning (IPC) had been found to be the most promising strategies against I/R injury. However, the potential molecular mechanisms underlying the protective effect of IPC have not been fully disclosed. MicroRNA182 (miR-182) is closely related to apoptosis and plays an important role in I/R injury. Our recent study demonstrated that miR-182 was down-regulated in the intestinal mucosa after I/R injury. However, whether miR-182 is involved in the protective effects of IPC in the setting of intestinal I/R injury is unknown., Aims: To investigate the role of miR-182 in the protective effect of IPC in intestine after I/R injury and potential mechanisms., Methods: AntagomiR-182 was pretreated before IPC in mice with intestinal I/R injury. MiR-182 mimic was administered before oxygen and glucose deprivation and reperfusion (OGD/R) in mice intestinal mucosa epithelial (MIME) cells., Results: IPC partially prevented the downregulation of miR-182 in mice, which was blocked by pretreatment with antagomiR-182. Compared with the IPC group, pretreatment with antagomiR-182 further increased Chiu's scores and diamine oxidase activities. Meanwhile, apoptotic cells and cleaved caspase-3 expression were increased. Compared with the OGD/R group, pretreatment with miR-182 mimic prevented the downregulation of miR-182, improved cell survival, reduced apoptosis and cleaved caspase-3 expression in MIME cells., Conclusions: The downregulation of miR-182 was partially prevented by IPC, which was involved in IPC induced intestinal protection, and the mechanisms may be associated with inhibition of apoptosis., (Copyright © 2019 IMSS. Published by Elsevier Inc. All rights reserved.)

The biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused by renal IR. Then, the circTLK1 expression level in HK-2 cells treated with OGD/R was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Functional experiments were performed with circTLK1 knockdown of HK-2 cells via Cell Counting Kit-8 (CCK8), flow cytometry (FCM), RT-qPCR, and western blotting. The circTLK1-miRNAs-mRNAs network was constructed following the ceRNA mechanism and visualized by Cytoscape software to investigate the mechanism of circTLK1 in AKI. RT-qPCR was performed to verify the relationship between circTLK1, miR-136-5p, and Bcl2. The level of miR-136-5p was knocked down to ensure its function in OGD/R-triggered apoptosis through experiments, including CCK8, FCM, RT-qPCR, and western blotting. CircTLK1 was downregulated in HK-2 cells subjected to OGD/R treatment and in mouse kidney tissues after renal IR, but the expression of miR-136-5p was the opposite. Interference with circTLK1 expression accelerated HK-2 cell apoptosis, which was overturned by miR-136-5p inhibitors. CircTLK1 targets miR-136-5p to upregulate Bcl2 expression and attenuate apoptosis in HK-2 cells. These data revealed the possible role of circTLK1 as a new biomarker for diagnosis as well as a target in AKI through the miR-136-5p/Bcl2 signaling axis. [ABSTRACT FROM AUTHOR]

Purpose. Sevoflurane, one of the most used general anesthetics, is widely used in clinical practice all over the world. Previous studies indicated that sevoflurane could induce neuron apoptosis and neural deficit causing query in the safety of anesthesia using sevoflurane. The present study was designed to investigate the effects of sevoflurane on electrophysiology in Drosophila pupa whose excitatory neurotransmitter is acetylcholine early after sevoflurane exposure using whole brain recording technique. Methods. Wide types of Drosophila (canton-s flies) were allocated to control and sevoflurane groups randomly. Sevoflurane groups (1% sevoflurane; 2% sevoflurane; 3% sevoflurane) were exposed to sevoflurane and the exposure lasted 5 hours, respectively. All flies were subjected to electrophysiology experiment using patch clamp 24 hours after exposure. Results. The results showed that, 24 hours after sevoflurane exposure, frequency but not the amplitude of miniature excitatory postsynaptic currents (mEPSCs) was significantly reduced P<0.05. Furthermore, we explored the underlying mechanism and found that calcium currents density, which partially regulated the frequency of mEPSCs, was significantly reduced after sevoflurane exposure P<0.05. Conclusions. All these suggested that sevoflurane could alter the mEPSCs that are related to synaptic plasticity partially through modulating calcium channel early after sevoflurane exposure. [ABSTRACT FROM AUTHOR]