Protective Effects of Sesamol against Liver Oxidative Stress and Inflammation in High-Fat Diet-Induced Hepatic Steatosis
| Autor: | Wenya Zheng, Ziyu Song, Sha Li, Minmin Hu, Horia Shaukat, Hong Qin |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Inflammation
Male Nutrition and Dietetics Nutrition. Foods and food supply Superoxide Dismutase hepatic steatosis Body Weight sesamol oxidative stress inflammation Diet High-Fat Antioxidants Article Mice Inbred C57BL Mice Oxidative Stress Liver Phenols Non-alcoholic Fatty Liver Disease Malondialdehyde Animals TX341-641 Benzodioxoles Energy Intake Biomarkers Food Science |
| Zdroj: | Nutrients; Volume 13; Issue 12; Pages: 4484 Nutrients Nutrients, Vol 13, Iss 4484, p 4484 (2021) |
| ISSN: | 2072-6643 |
| DOI: | 10.3390/nu13124484 |
| Popis: | Chronic high-fat diet (HFD) is associated with the onset and progression of hepatic steatosis, and oxidative stress is highly involved in this process. The potential role of sesamol (SEM) against oxidative stress and inflammation at the transcriptional level in a mice model of hepatic steatosis is not known. In this study, we aimed to investigate the scavenging effects of SEM towards reactive oxygen generated by lipid accumulation in the liver of obese mice and to explore the mechanisms of protection. Markers of oxidative stress, vital enzymes involved in stimulating oxidative stress or inflammation, and nuclear transcription of Nrf2 were examined. Our results showed that SEM significantly inhibited the activity of the HFD-induced hepatic enzymes CYP2E1 and NOX2, associated with oxidative stress generation. Additionally, SEM reversed HFD-induced activation of NF-κB, a redox-sensitive transcription factor, and attenuated the expression of hepatic TNF-α, a proinflammatory molecule. Moreover, SEM enhanced HFD-induced hepatic Nrf2 nuclear transcription and increased the levels of its downstream target genes Ho1 and Nqo1, which indicated antiinflammation and antioxidant properties. Our study suggests that chronic HFD led to hepatic steatosis, while SEM exhibited protective effects on the liver by counteracting the oxidative stress and inflammation induced by HFD. The underlying mechanism might involve multiple pathways at the transcriptional level; the antioxidant defense mechanism was in partly mediated by the upregulation of Nrf2. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|