Browsing by Subject "Sevoflurane"

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    MicroRNA-204-5p mediates sevoflurane-induced cytotoxicity in HT22 cells by targeting brain-derived neurotrophic factor
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Wang, Jun; Wang, Jun; Yan, Rongrong; Jin, Shuangfen; Wan, Zhenzhen; Cheng, Jing; Li, Na; Chen, Lin; Le, Chengjin
    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
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    Sevoflurane suppresses hepatocellular carcinoma cell progression via circ_0001649/miR-19a-3p/SGTB axis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Sun, Nai; Gong, Jianzhuang; Zhang, Wei; Yang, Xiaochen; Liu, Jiaying
    Background. Sevoflurane is a widely used anesthetic agent and is reported to play an anti-tumor action in many cancers. However, the underlying mechanisms are largely unclear. Methods. Hepatocellular carcinoma (HCC) cells were treated with sevoflurane for 12 or 24 h. HCC cell proliferation, migration, invasion, and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-ethynyl-2’- deoxyuridine (EdU) assay, transwell assay, and flow cytometry assay, respectively. The protein levels were determined by western blot. The expression of circular RNA (circ)_0001649, microRNA (miR)-19a-3p, and small glutamine rich tetratricopeptide repeat containing Beta (SGTB) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between miR-19a-3p and circ_0001649 or SGTB was predicted by Starbase and confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results. Sevoflurane inhibited HCC cell proliferation, migration, and invasion, but promoted apoptosis. Sevoflurane could affect the expression of circ_0001649 and knockdown of circ_0001649 reversed the effects of sevoflurane on HCC cell progression. Subsequently, miR-19a-3p was identified as a target of circ_0001649 and directly targeted SGTB. In addition, circ_0001649 suppressed the development of sevoflurane-induced HCC cells through miR-19a3p/SGTB axis. Conclusion. Our study demonstrated that sevoflurane inhibited HCC cell development via circ_0001649/miR-19a-3p/SGTB axis