Objective:To observe the analgesic efficacy of fascia iliaca compartment block with dexmedetomidine and ropivacaine under general anesthesia for pediatric patients with femoral fracture.Methods:Sixty-four children, 6-10 years old, ASA ⅠorⅡ, underwent open reduction and internal fixation for femoral fracture under general anesthesia combined with fascia iliaca comparment block from July 2020 to December 2021, were collected. The children were randomly divided into dexmedetomidine and ropivacaine group (group DR, n=32) and ropivacaine alone group (group R, n=32). The children received iliofascia compartment block with 0.25% ropivacaine 0.5 ml/kg combined with 1 μg/kg dexmedetomidine in the group DR, and received 0.25% ropivacaine 0.5 ml/kg in the group R respectively. FLACC pain scores were recorded at 2, 6, 12, 18, 24 h after the operation. The duration of block and the dose of tramadol within 24 h after the operation were observed, and the occurrence of agitation and adverse reactions (nerve injury, bradycardia, nausea and vomiting, excessive sedation) during the recovery period were recorded. Results:Compared with the group R, FLACC score was lower in the group DR at 6 h (Wald χ2=33.09, P<0.001), 12 h (Wald χ2=50.02, P<0.001) and 18 h (Wald χ2=42.00, P<0.001) after the operation. The duration of block was significantly longer in the group DR than that in the group R ( Z=-6.66, P<0.001). Compared with the group R, the number of patients requiring tramadol for relief pain at 24 h after the operation in the group DR was fewer ( χ2=4.63, P=0.031), and the dosage of tramadol was also lower ( t=6.54, P<0.001). The incidence of agitation, nausea and vomiting were less in the group DR than that in the group R (3 cases vs. 11 cases, χ2=5.96, P=0.015), (2 cases vs. 9 cases, χ2=5.46, P=0.020) respectively. The incidence of bradycardia was identical between the two groups ( P>0.05). Conclusion:Dexmedetomidine 1 μg/kg combined with ropivacaine for fascia iliaca compartment block during general anesthesia can reduce the agitation in recovery period, provide longer postoperative analgesia, lower the incidence of adverse reactions.

Purpose Sevoflurane (SEV) is a frequently used volatile anesthetic in cancer surgery. Sevoflurane treatment has been shown to suppress the migration and invasion of several human cancer cells. However, the effect of sevoflurane on glioma remains largely unclear. Methods Glioma cell lines (U251 and U343) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry assay, and transwell assay were performed to detect the cell viability, apoptosis, migration and invasion. Western blot assay was employed to detect the protein levels of β-catenin, c-Myc, CyclinD1, β-catenin, N-cadherin, vimentin, and DEK. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of miR-218-5p. The target interaction between miR-218-5p and DEK was predicted through bioinformatics analysis and verified by dual-luciferase reporter assay system. Results We found that sevoflurane aberrantly inhibited the abilities on viability, migration, invasion, EMT and β-catenin signaling and promoted cell apoptosis in U251 and U343 cells in a dose-dependent manner. MiR-218-5p strikingly suppressed the abilities of proliferation, migration, invasion rather than apoptosis and activation of β-catenin signaling. Sevoflurane could facilitate the miR-218-5p expression, and its suppressing effects on glioma cells were reversed by pre-treatment with miR-218-5p inhibitors or pcDNA3.1/DEK in vitro and in vivo. Silencing of miR-218-5p reverted sh-DEK and sevoflurane-induced repression on proliferation, migration, invasion, and β-catenin signaling, and promotion on apoptosis in the glioma cells. Conclusion Our data showed that sevoflurane inhibited the proliferation, migration, invasion, and enhanced the apoptosis in glioma cells through regulating miR-218-5p/DEK/β-catenin axis.

Abstract Background Interferon regulatory factor 8 (IRF8) is involved in the pathogenesis of neuropathic pain. However, whether and how IRF8 can regulate the nicotine withdrawal (NTW)-induced hyperalgesia has not been clarified. Methods C57BL/6 mice were randomized and injected subcutaneously with saline (Control) or nicotine (3 mg/kg) three times per day for 7 consecutive days, followed by injection with mecamylamine to induce NTW. Their paw withdrawal latencies (PWLs) were measured, and the relative levels of IRF8 expression in the spinal cord tissues were determined longitudinally by western blot. The numbers of IRF8+ cells in the spinal cord tissues were examined. In addition, the NTW mice were randomized and infused intrathecally with vehicle saline (NS), control lentivirus or lentivirus for the expression of IRF8-specific shRNA for three days. Their PWLs, microglia activation, IRF8 and P2X4R and BDNF expression in the spinal cord tissues were determined. Results In comparison with the Control mice, the NTW significantly decreased the PWLs but increased the relative levels of IRF8 expression and the numbers of IRF8+ cells in the spinal cord tissues of mice. IRF8-silencing significantly mitigated the NTW-decreased PWLs and attenuated the NTW-enhanced microglia activation and P2X4R and BDNF expression in the spinal cord tissues of mice. Conclusions Spinal IRF8 is crucial for the NTW-induced hyperalgesia by enhancing microglia activation and spinal P2X4R and BDNF expression in mice. The IRF8/P2X4R/BDNF axis may be potential therapeutic targets for postoperative pain of smokers.