Hydrogen attenuated oxidized low‑density lipoprotein‑induced inflammation through the stimulation of autophagy via sirtuin 1
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DOI:
10.3892/etm.2018.6691
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Abstract:
Chronic inflammation is a central pathogenic mechanism underlying the induction and progression of atherosclerosis (AS). Hydrogen has been demonstrated to serve a protective role in diverse models of disease. However, the potential effects and mechanism of hydrogen with respect to ox-LDL-induced inflammation have not yet been completely elucidated. In the present study, various concentrations (0, 50 and 100 mg/l) of oxidized low-density lipoprotein (ox-LDL) were used to treat RAW264.7 cells. A Cell Counting kit-8 assay was used to determine cell viability and western blot analysis was performed to determine the expression of proteins that are involved in autophagy. The expression of inflammatory cytokines in ox-LDL-treated macrophages was detected using ELISA. Small interfering (si)RNA against sirtuin 1 (SIRT1) was employed to investigate the mechanism underlying hydrogen-activated autophagy. The results indicated that ox-LDL stimulation promoted inflammatory cytokine expression and impaired autophagic flux in RAW264.7 cells. Furthermore, hydrogen inhibited ox-LDL-induced inflammatory cytokine expression by upregulating autophagic flux. SIRT1 mediated the upregulation of autophagic flux via hydrogen in ox-LDL-treated macrophages. To conclude, the present study provided novel insights into the role of defective autophagy in the pathogenesis of AS and identified autophagy to be a promising therapeutic target for the treatment of AS. Notably, hydrogen may represent a potential agent for the treatment of AS.| Publish Year | 2018 |
|---|---|
| Country | China |
| Rank | Positive |
| Journal | Experimental and Therapeutic Medicine |
| Primary Topic | Heart |
| Secondary Topic | Atherosclerosis |
| Model | Cell Culture |
| Tertiary Topic | Inflammation |
| Vehicle | Medium (Dissolved) |
| pH | Neutral |
| Application | Culture Media |
| Comparison | |
| Complement |