Department of Medicine, Faculty of Chinese Medicine Science, Guangxi University of Chinese Medicine, Nanning 530222, China
| Abstract: | Objective: To analyze the molecular mechanism of lncRNA NEAT1 regulation of liver fibrosis with the help of bioinformatics and experimental validation, hoping to provide new ideas for the prevention and treatment of liver fibrosis and drug development. Methods: Screening lncRNA NEAT1 target miRNAs with the help of Starbase database; screening miRNA target mRNAs using miRDB database; obtaining liver fibrosis-related targets through OMIM, CTD and GeneCards databases; interacting lncRNA NEAT1 regulatory targets with liver fibrosis targets, and performing key target Enrichment analysis was performed. Hepatic stellate cells (HSC) were activated with LPS and divided into blank and model groups. HSC were transfected with siNEAT1 and negative control and divided into siNEAT1 NC+LPS and siNEAT1+LPS. MTT method was used to detect the proliferation of HSC and flow cytometry was used to detect the apoptosis rate of HSC; molecular biology was used to detect α-SMA and Collagen I expression. Results: lncRNA NEAT1 targeted 26 miRNA molecules, miRNA targeted 564 mRNAs, 617 liver fibrosis-related targets, lncRNA NEAT1 regulated 20 key targets of liver fibrosis, lncRNA NEAT1 involvement in liver fibrosis may be closely related to its regulation of cellular senescence. lncRNA NEAT1 expression increased significantly upon HSC activation. The proliferation rate of HSC cells was significantly decreased and apoptosis rate was significantly increased after NEAT1 silencing, and the expression of α-SMA and Collagen I was also significantly decreased. Conclusion: NEAT1 is involved in the development of liver fibrosis by regulating HSC proliferation and apoptosis, and may be closely related to its involvement in the ceRNA network that regulates cellular senescence. |
| Keywords: | lncRNANEAT1; ceRNA; Apoptosis; Senescence; Hepatic Stellate Cells; Hepatic Fibrosis |
| DOI: | 10.57237/j.life.2023.01.003 |
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