Efficacy of Analgesic Propofol/Esketamine and Propofol/Fentanyl for Painless Induced Abortion: A Randomized Clinical Trial.

Background: Patients have widely accepted abortion as a remedy for contraceptive failure all over the world. Esketamine is a new anesthetic, sedative, and analgesic drug. Fentanyl is an opioid receptor agonist and a commonly used sedative. It is necessary to choose appropriate sedative drugs for painless abortion. Methods: We selected 238 cases of painless induced abortion from January 2020 to January 2022. We collected surgical parameters, the performance of sedation, and postoperative scales with complications before and after the operation. SPSS 21.0 was used to analyze data. Results: Surgical indicators between intervention and control groups had no difference; the preoperative indicators including intraoperative bispectral index (BIS), systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse oxygen saturation (SpO2) had no difference between the two groups. But after surgery, experiment groups had a higher value than the control group in these four indicators. The incidence of postoperative complications including nausea and vomit had no significant difference while the experiment group had a lower r-value than the control group in hypotension, bradycardia, decreased oxygen saturation, and respiratory depression. The postoperative VAS score and Ramsay score in the experimental group were lower than those in the control group. Conclusion: Since esketamine had better sedation performance, reduce the risk of cardiovascular and respiratory depression during sedation, and reduce the pain scale compared with fentanyl, we supported that propofol/esketamine is a good choice for patients receiving a painless induced abortion, and it is a sedation plan worth promoting and further analysis.

Dexmedetomidine inhibits cell malignancy in osteosarcoma cells via miR-520a-3p-YOD1 interactome.

BACKGROUND: Osteosarcoma is a common malignant tumor in adolescents with a low 5-year survival rate. Dexmedetomidine (DEX) has been widely used for surgery of osteosarcoma patients. MiR-520a-3p and YOD1 expression was abnormal in osteosarcoma cells. However, whether DEX affects osteosarcoma progression via miR-520a-3p-YOD1 interactome needs to be explored. METHODS: We detected osteosarcoma cells biological behavior by CCK-8 assay, BrdU assay, cell adhesion assay, and apoptosis assay, respectively. The miR-520a-3p and YOD1 levels was explored in osteosarcoma cell lines by RT-qPCR or western blotting assay. RESULTS: In this study, we found that DEX treating osteosarcoma cells inhibited cell viability, proliferation and adhesion, while it promoted cell apoptosis. Moreover, miR-520a-3p targeting to YOD1 also functionally repressed cell malignancy in osteosarcoma cells. Notably, DEX treatment could inhibit YOD1 expression via upregulating miR-520a-3p, thereby suppressing cell malignancy in osteosarcoma. CONCLUSIONS: Our study first revealed that DEX inhibited malignancy of osteosarcoma cells via miR-520a-3p/YOD1 axis.

MicroRNA-204-5p mediates sevoflurane-induced cytotoxicity in HT22 cells by targeting brain-derived neurotrophic factor.

BACKGROUND: Sevoflurane is widely used as an inhalational anesthetic in clinical practice. However, sevoflurane can cause cytotoxicity and induce learning capacity decline in patients. A previous publication indicated that miR-204-5p might have a close relationship with sevoflurane-induced neurotoxicity. When exposed to sevoflurane, the expression of miR-204-5p in neonatal hippocampus of rats was significantly increased. Hence, we aimed to investigate the role of miR-204-5p in sevoflurane-induced neurotoxicity using a mouse hippocampal neuronal cell line (HT22). METHODS: The levels of miR-204-5p in HT22 cells were detected by RT-qPCR. In addition, the effects of miR-204-5p on cell viability, apoptosis and proliferation were evaluated by CCK-8, flow cytometric, and immunofluorescence assay, respectively. Western blotting was used to detect expressions of Bax, Bcl-2, active caspase 3, BDNF, TrkB, p-TrkB, Akt and p-Akt in HT22 cells. ELISA assay was used to examine the levels of total superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde (MDA) and reactive oxygen species (ROS) in cells. Meanwhile, the dual luciferase reporter system assay was employed to explore the interaction of miR-204-5p and BDNF in cells. RESULTS: The level of miR-204-5p was increased in sevoflurane-treated HT22 cells. Moreover, downregulation of miR-204-5p inhibited sevoflurane-induced apoptosis and promoted cell proliferation by upregulating the proteins of Bcl-2 and downregulating the expressions of Bax and active caspase-3 in HT22 cells. In addition, inhibition of miR-204-5p alleviated sevoflurane-induced oxidative injuries in HT22 cells via decline of ROS and MDA and upregulation of SOD and GSH. Furthermore, bioinformatics and dual luciferase assay demonstrated that miR-204-5p can inhibit the TrkB/Akt pathway by targeting BDNF. CONCLUSION: Our findings indicated that downregulation of miR-204-5p can decrease oxidative status in HT22 cells and alleviate sevoflurane-induced cytotoxicity through stimulating the BDNF/TrkB/Akt pathway. Therefore, miR-204-5p might be a potential biomarker and therapeutic target for the treatment of sevoflurane-induced neurotoxicity.