Publication:
Propofol protects PC12 cells from cobalt chloride-induced injury by mediating miR-134

dc.contributor.authorZhou, Hong-Yi
dc.contributor.authorJiang, Fan
dc.contributor.authorCao, Zhong
dc.contributor.authorShen, Qi-Yun
dc.contributor.authorFeng, Yu-Jing
dc.contributor.authorHou, Zhen-Huan
dc.date.accessioned2023-01-11T16:54:41Z
dc.date.available2023-01-11T16:54:41Z
dc.date.issued2021
dc.description.abstractObjective. Propofol (PRO) was reported to exert a neuroprotective effect by decreasing microRNA134 (miR-134), a brain-specific miRNA, thus, the role of PRO against cobalt chloride (CoCl 2)-induced injury in rat pheochromocytoma cells (PC12) via mediating miR134 was explored. Methods. CoCl 2-induced PC12 cells treated with PRO were transfected with or without miR-134 negative control (NC)/ inhibitor/mimic, and the following detections were then performed using cell counting kit-8 (CCK-8), Annexin V-fluorescein isothiocyanate/ propidium iodide (Annexin V-FITC/PI) and Hoechst 33258 staining. Autophagy was observed by transmission electron microscope (TEM). Mitochondrial membrane potential (MMP) was detected by Rhodamine-123 (Rh123) staining, and reactive oxygen species (ROS) by dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining. Protein and gene expressions were measured by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Results. PRO reversed the CoCl 2-induced decrease in the PC12 cell viability and increased miR-134 in a dose-dependent manner. CoCl 2 increased LC3II/I ratio and Beclin-1 expression, but decreased p62 expression, which was abolished by PRO. In addition, an increased cell apoptosis rates triggered by CoCl 2 were reduced by PRO with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2. Furthermore, PRO decreased methylenedioxyamphetamine (MDA), nitric oxide (NO) and ROS in CoCl 2-induced PC12 cells accompanying the increase in glutathione peroxidase (GSH-Px) and MMP. The effects of PRO on autophagy, apoptosis and oxidative stress in CoCl 2-induced PC12 cell were reversed by miR-134 mimic. Conclusion. PRO may mitigate CoCl2-induced autophagy in PC12 cells with decreased apoptosis and improved oxidative stress via mediating miR-134.es
dc.formatapplication/pdfes
dc.format.extent11es
dc.identifier.citationHistology and Histopathology Vol. 36, nº4 (2021)
dc.identifier.doihttps://doi.org/10.14670/HH-18-298
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/127144
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectPropofoles
dc.subjectMicroRNA-134es
dc.subjectPC12es
dc.subjectCobalt chloridees
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titlePropofol protects PC12 cells from cobalt chloride-induced injury by mediating miR-134
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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