ABSTRACT
Resumo A aterosclerose é a causa mais comum de doença cardiovascular em todo o mundo, ela está associada a uma alta incidência de eventos clínicos. O acúmulo de evidências elucidou que os RNAs longos não codificantes (LncRNAs) são uma nova classe de transcritos com papéis críticos nos processos fisiopatológicos da aterosclerose. Nesta revisão, resumimos o progresso recente dos LncRNAs no desenvolvimento da aterosclerose. Descrevemos principalmente os diversos mecanismos regulatórios dos LncRNAs nos níveis transcricionais e pós-transcricionais. Este estudo pode fornecer informações úteis sobre os LncRNAs como alvos terapêuticos ou biomarcadores para o tratamento da aterosclerose.
Abstract Atherosclerosis is the most common cause of cardiovascular disease globally, associated with a high incidence of clinical events. Accumulating evidence has elucidated that long non-coding RNAs (lncRNAs) as a novel class of transcripts with critical roles in the pathophysiological processes of atherosclerosis. In this review, we summarize the recent progress of lncRNAs in the development of atherosclerosis. We mainly describe the diverse regulatory mechanisms of lncRNAs at the transcriptional and post-transcriptional levels. This study may provide helpful insights about lncRNAs as therapeutic targets or biomarkers for atherosclerosis treatment.
ABSTRACT
This study is to investigate the cytoprotective role of NaNO2 preconditioning against ethanol induced damage in human hepatoma SMMC-7721 cells. The cells were preconditioned with NaNO2 (0.25 mmol x L(-1)) for 24 hours or 4 weeks, and then exposed to ethanol (200 mmol x L(-1)) for additional 12 h and untreated cells served as control. Both temporal and chronic NaNO2 preconditioning could prevent ethanol elicited cytotoxicity as evidenced by thiazolyl blue (MTT). NaNO2 preconditioning also could inhibit ethanol-induced apoptosis, which was confirmed by FITC-Annexin V/PI flow cytometer and Hoechst 33258 and PI staining. Further, simultaneous NaNO2 preconditioning treatment along with ethanol showed protection against ethanol mediated cellular damage as indicated by significantly decreased levels of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD) and catalase (CAT). Western blotting analysis revealed that in ethanol treated cells preconditioned with NaNO2, the HIF-1alpha and Bcl-2 increased obviously, while the expression of pro-apoptotic proteins, including Bax, Caspase-9, Caspase-3 decreased. The results showed that low doses of NaNO2 preconditioning resistant to ethanol-induced human hepatoma SMMC-7721 cells apoptosis, which mechanism may be related to increased expression of HIF-1alpha in the cells.