Upstream stimulating factor 2 aggravates neuropathic pain induced in spinal nerve ligation-induced mice via regulating SNHG5/miR-181b-5p.

BACKGROUND: Upstream stimulating factor 2 (USF2) belongs to basic-Helix-Loop-Helix-Leucine Zipper transcription factor family, regulating expression of genes involved in immune response or energy metabolism network. Role of USF2 in neuropathic pain was evaluated. METHODS: Mice were intraspinally injected with adenovirus for knockdown of USF2 (Ad-shUSF2), and then subjected to spinal nerve ligation (SNL) to induce neuropathic pain. Distribution and expression of USF2 was detected by western blot and immunofluorescence. Mechanical and thermal pain sensitivity were examined by paw withdrawal thresholds (PWT) and paw withdrawal latency (PWL). Chromatin immunoprecipitation (ChIP) and luciferase activity assays were performed to detect binding ability between USF2 and SNHG5. RESULTS: The expression of USF2 was elevated and colocalized with astrocytes and microglia in L5 dorsal root ganglion (DRG) of SNL-induced mice. Injection of Ad-shUSF2 attenuated SNL-induced decrease of PWT and PWL in mice. Knockdown of USF2 increased level of IL-10, but decreased TNF-α, IL-1ß, and IL-6 in SNL-induced mice. Silence of USF2 enhanced protein expression of CD206, while reduced expression of CD16 and CD32 in SNL-induced mice. USF2 bind to promoter of SNHG5, and weakened SNL-induced up-regulation of SNHG5. SNHG5 bind to miR-181b-5p, and miR-181b-5p to interact with CXCL5. CONCLUSION: Silence of USF2 ameliorated neuropathic pain, suppressed activation of M1 microglia and inhibited inflammation in SNL-induced mice through regulation of SNHG5/miR-181b-5p/CXCL5 axis. Therefore, USF2/SNHG5/miR-181b-5p/CXCL5 might be a promising target for neuropathic pain. However, the effect of USF2/SNHG5/miR-181b-5p/CXCL5 on neuropathic pain should also be investigated in further research.

Interfacial self-healing polymer electrolytes for Long-Cycle silicon anodes in High-Performance solid-state lithium batteries.

For all-solid-state lithium-ion batteries (ASSLIBs), silicon (Si) stands out as an appealing anodes material due to its high energy density and improved safety compared to lithium metal. However, the substantial volume changes during cycling result in poor solid-state physical contact and electrolyte-electrode interface issues, leading to unsatisfactory electrochemical performance. In this study, we employed in-situ polymerization to construct an integrated Si anodes/self-healing polymer electrolyte for ASSLIBs. The polymer chain reorganization stems from numerous dynamic bonds in the constructed self-healing dynamic supermolecular elastomer electrolyte (SHDSE) molecular structure. Notably, SHDSE also serves as a Si anodes binder with enhanced adhesive capability. As a result, the well-structured Li|SHDSE|Si-SHDSE cell generates subtle electrolyte-electrode interface contacts at the molecular level, which can offer a continuous and stable Li+ transport pathway, reduce Si particle displacement, and mitigate electrode volume expansion. This further enhances cyclic stability (>500 cycles with 68.1 % capacity retention and >99.8 % Coulombic efficiency). More practically, the 2.0 Ah wave-shaped Si||LiCoO2 soft-pack battery with in-situ cured SHDSE exhibits strongly stabilized electrochemical performance (1.68 Ah after 700 cycles, 86.2 % capacity retention) in spite of a high operating temperatures up to 100 °C and in various bending tests. This represents a groundbreaking report in flexible solid-state soft-pack batteries containing Si anodes.

The closed-loop recycling strategy of Li and Co metal ions based on aqueous Zn-air desalination battery.

Nowadays, it is a global problem to recycle LiCoO2 from waste lithium-ion batteries (LIBs) due to the deficiency of high business cost and environmental pollution. Here, a novel three-channel ion recovery device based on a Zn-air desalination battery (ZADB) is proposed which can supply energy while separating Li+ and Co2+ from the recovered solution. The three-channel ZADB device consists of a Zn foil anode chamber with ZnSO4 anolyte stream, an intermediate chamber with Li+ and Co2+ recovered stream and an air cathode chamber with LiOH and Co(OH)2 catholyte stream, chambers are separated by anion exchange membrane (AEM) and cation exchange membrane (CEM) respectively. It can be described by the finite element simulation (FES) of physics field that, the Li+ and Co2+ in the recovered solution move to the cathode chamber, where the OH- are produced by absorbing O2 from the air combined with electronic in the discharge process. At the same time, the SO42- moves to the other end of the Zn foil anode chamber according to the law of charge conservation, which combined with the Zn2+ removed from the Zn foil. The results show that the recovery efficiency of the ZADB device is closely related to the discharge current density and the concentration of the recovered stream. The best recovery effect has achieved when 0.2 mol L-1 recovered solution is run for 24 h at the discharge current density of 0.2 mA cm-2. The average recovery rate is 0.275 mg min-1 with the highest recovery rate is 40.73 mg h-1, and the output energy density is 102.5 Wh Kg-1 during the experiment process. In addition, the ZADB device has the excellent long-term cycling performance and recycling stability. By comparing this device with other ion recovery methods, which provides that it is a splendid way to recycle Li+ and Co2+ from waste LIBs.

Protection of propofol on liver ischemia reperfusion injury by regulating Cyp2b10/ Cyp3a25 pathway.

To verify whether propofol alleviates liver ischemia-reperfusion injury (IRI) in mice by regulating Cyp2b10/ Cyp3a25 pathway. The liver I/R injury in vivo and in vitro model was constructed. The serum level of AST, ALT, ALP and ALB was detected using ELISA. The mRNA and protein expression of Cyp2b10 and Cyp3a25 were determined by qRT-PCR and western blot, respectively. The liver cell activity was assessed by MTT assay. The binding between Cyp2b10 and Cyp3a25 was evaluated by online website prediction, CoIP, and cell transfection with Cyp2b10 siRNA and pcDNA3.1-Cyp3a25. The hepatocyte apoptosis was examined using flow cytometry assay. The serum level of AST, ALT, ALP was increased and that of ALB was decreased in liver I/R injury in vivo model. Also, the mRNA and protein expression of Cyp2b10 and Cyp3a25 were enhanced and reduced in liver I/R injury in vivo and vitro model respectively. The liver cell activity was markedly reduced in H/R cell model. However, these changes were all reversed with propofol treatment. Furthermore, Cyp2b10 could directly bind to Cyp3a25 to regulate the H/R-induced hepatocyte apoptosis. Propofol plays an effect of on liver I/R injury by regulating Cyp2b10/ Cyp3a25 pathway.

The hepatoprotective effect from ischemia-reperfusion injury of remote ischemic preconditioning in the liver related surgery: a meta-analysis.

BACKGROUND: This study aimed to assess the hepatoprotective effect of remote ischemic preconditioning (RIPC) in the liver related surgery. METHODS: Published articles in PubMed, Embase and Cochrane clinical trial databases were searched from the inception to May 2021. Randomized control trials (RCTs) comparing the RIPC with control or other conditionings were included for analysis. The postoperative liver synthetic function was used as the primary outcome. RESULTS: A total of six RCTs were included the present meta-analysis. There were 216 patients underwent RIPC and 212 patients in the control group. The RIPC group had a significantly lower level of postoperative alanine transaminase and aspartate transaminase (p<0.001). The postoperative bilirubin level was also significant lower in the RIPC group than the control group (MD = -9.0, 95%CI, -13.94 to -4.03; p<0.001). ICG clearance was reduced in controls versus RIPC (p<0.001). There was no significant difference between the RIPC and control group in terms of the complication rate. CONCLUSION: The RIPC was evaluated to have a strong hepatoprotective effect from ischemia-reperfusion injury in the liver related surgery.

Long Noncoding RNA SNHG5 Knockdown Alleviates Neuropathic Pain by Targeting the miR-154-5p/CXCL13 Axis.

Neuropathic pain is an unneglectable pain condition with limited treatment options owing to its enigmatic underlying mechanisms. Long noncoding RNA small nucleolar RNA host gene 5 (SNHG5) is involved in the progression of a spectrum of human cancers. However, its role in neuropathic pain remains undiscovered. In the present study, we established a mouse spinal nerve ligation (SNL) model, and a significant upregulation of SNHG5 was observed. Then we knocked down SNHG5 level in mouse L5 dorsal root ganglion (DRG) by delivering specific short hairpin RNA against SNHG5 with adenovirus vehicle. Mouse paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in response to mechanical stimuli was increased after SNHG5 knockdown, accompanied with decreased protein levels of glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecule 1 (IBA-1). Besides, SNHG5 directly modulated the expression of miR-154-5p, which was downregulated in SNL mice. MiR-154-5p inhibition abolished the effect of SNHG5 knockdown on mouse behavioral tests and GFAP and IBA-1 levels. In addition, we validated that C-X-C motif chemokine 13 (CXCL13) was a novel downstream target of miR-154-5p, and CXCL13 level was positively related to that of SNHG5 in SNL mice. In conclusion, our study demonstrated that SNHG5 knockdown alleviated neuropathic pain and inhibited the activation of astrocytes and microglia by targeting the miR-154-5p/CXCL13 axis, which might be a novel therapeutic target for neuropathic treatment clinically.

Isoflurane pre-treatment before cardiopulmonary bypass alleviates neutrophil accumulation in dog lungs.

OBJECTIVE: This study investigated the effect of isoflurane pretreatment on cardiopulmonary bypass (CPB)-related lung injury. METHODS: Twelve dogs were randomly divided into two groups of six each. In one group, 1.0 minimum alveolar concentration (MAC) of isoflurane was dministered for 30 min before CPB, while the control group received no anaesthetic. Both groups then underwent 100 min of mild hypothermic CPB with 60-min aortic cross clamping. Haemodynamic parameters, respiratory mechanics and alveolar arterial oxygen difference (AaDO2) were measured during the experiment. One hundred and fifty minutes after CPB, lung tissue samples from the non-dependent and dependent portions of the left and right lungs were harvested for polymorphonulear leukocyte (PMNs) counts. RESULTS: Following CPB, within the control group, pulmonary vascular resistance (PVR) was significantly increased at 60, 120 and 180 min after declamping, AaDO2 deteriorated at 180 min post-declamping, and dynamic lung compliance (DLC) was reduced dramatically after declamping. Isoflurane pretreatment before CPB significantly reduced PVR compared to the controls. AaDO2 was impaired at 180 min after declamping and DLC was decreased after declamping within the isoflurane group. No differences in AaDO2 and DLC were found between the isoflurane and control groups. At 180 min after declamping, the PMN count in both the non-dependent and dependent regions of the isoflurane pre-treated lungs was significantly lower than that of the controls. CONCLUSIONS: Our results suggest that 30-min pre-treatment with 1.0 MAC isoflurane before CPB caused a reduction in PMN accumulation in the dog lungs, inhibition of increases in PVR, and it did not affect AaDO2 in the early post-CPB stage.