Propofol alleviates oxidative stress via upregulating lncRNA-TUG1/Brg1 pathway in hypoxia/reoxygenation hepatic cells
| Autor: | Ha Sen Ta Na, Nuo Ming, Qing-Tao Meng, Zhongyuan Xia, Jin-Ling He |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
Immunoprecipitation Pharmacology medicine.disease_cause Biochemistry 03 medical and health sciences Mice 0302 clinical medicine Downregulation and upregulation medicine Gene silencing Animals Viability assay Hypoxia Molecular Biology Propofol 030304 developmental biology 0303 health sciences Chemistry DNA Helicases Nuclear Proteins General Medicine Hypoxia (medical) medicine.disease Up-Regulation Mice Inbred C57BL Oxygen Oxidative Stress 030220 oncology & carcinogenesis Hepatic stellate cell Hepatocytes RNA Long Noncoding medicine.symptom Reperfusion injury Oxidative stress Transcription Factors |
| Zdroj: | Journal of biochemistry. 166(5) |
| ISSN: | 1756-2651 |
| Popis: | Reducing oxidative stress is an effective method to prevent hepatic ischaemia/reperfusion injury (HIRI). This study focuses on the role of propofol on the oxidative stress of hepatic cells and the involved lncRNA-TUG1/Brahma-related gene 1 (Brg1) pathway in HIRI mice. The mouse HIRI model was established and was intraperitoneally injected with propofol postconditioning. Hepatic injury indexes were used to evaluate HIRI. The oxidative stress was indicated by increasing 8-isoprostane concentration. Mouse hepatic cell line AML12 was treated with hypoxia and subsequent reoxygenation (H/R). The targeted regulation of lncRNA-TUG1 on Brg1 was proved by RNA pull-down, RIP (RNA-binding protein immunoprecipitation) and the expression level of Brg1 responds to silencing or overexpression of lncRNA-TUG1. Propofol alleviates HIRI and induces the upregulation of lncRNA-TUG1 in the mouse HIRI model. Propofol increases cell viability and lncRNA-TUG1 expression level in H/R-treated hepatic cells. In H/R plus propofol-treated hepatic cells, lncRNA-TUG1 silencing reduces cell viability and increased oxidative stress. LncRNA-TUG1 interacts with Brg1 protein and keeps its level via inhibiting its degradation. Brg1 overexpression reverses lncRNA-TUG1 induced the reduction of cell viability and the increase in oxidative stress. LncRNA-TUG1 silencing abrogates the protective role of propofol against HIRI in the mouse HIRI model. LncRNA-TUG1 has a targeted regulation of Brg1, and thereby affects the oxidative stress induced by HIRI. This pathway mediates the protective effect of propofol against HIRI of hepatic cell. |
| Databáze: | OpenAIRE |
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