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Published on: August 31, 2015
Aucubin inhibited lipid accumulation and oxidative stress via Nrf2/HO-1 and AMPK signalling pathways
Bingyu Shen1, Chenxu Zhao1, Yue Wang2
1Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, Jilin, PR China.
Abstract:
Aucubin (AU) is the main active ingredient of Aucuba japonica which has showed many positive effects such as anti-inflammation and liver protection. Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. In this research, we explored the effects of AU on the tyloxapol-induced NAFLD in mice and apolipoprotein C-III (apoC-III) induced-3T3L1 cells. Tyloxapol (300 mg/kg) was injected to C57BL/6 mice with aucubin. The differentiated 3T3-L1 cells were treated with or without aucubin after stimulation of apoC-III (100 μg/mL). In results, aucubin inhibited hyperlipidaemia, oxidative stress and inflammation by influencing the content of total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), very low density lipoprotein (VLDL), myeloperoxidase (MPO), superoxide dismutase (SOD), tumour necrosis factor receptor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in blood. AU activated NF-E2-related factor 2 (Nrf2), peroxisome proliferator-activated receptor α (PPARα), PPARγ and hemeoxygenase-1 (HO-1) and promoted the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPKα), AMPKβ, acetyl-CoA carboxylase (ACC) and protein kinase B (AKT). In conclusion, AU performed the function of hypolipidaemic by its obvious anti-inflammation and antioxidant activity, which may become a kind of new drug targeting at NAFLD.
Insights
Aucubin (AU) effectively combats non-alcoholic fatty liver disease (NAFLD) by reducing lipids, inflammation, and oxidative stress. This natural compound shows promise as a novel therapeutic agent for liver health.
Area of Science:
- Pharmacology
- Hepatology
- Biochemistry
Background:
- Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition.
- Aucubin (AU), derived from Aucuba japonica, possesses known anti-inflammatory and liver-protective properties.
Purpose of the Study:
- To investigate the therapeutic effects of Aucubin (AU) on non-alcoholic fatty liver disease (NAFLD).
- To evaluate AU's impact on tyloxapol-induced NAFLD in mice and apolipoprotein C-III (apoC-III) induced 3T3-L1 cells.
Main Methods:
- Administration of tyloxapol and Aucubin (AU) to C57BL/6 mice.
- Treatment of differentiated 3T3-L1 cells with AU following apolipoprotein C-III (apoC-III) stimulation.
- Analysis of biochemical markers including lipids, oxidative stress indicators, and inflammatory cytokines.
Main Results:
- Aucubin (AU) significantly inhibited hyperlipidemia, oxidative stress, and inflammation.
- AU modulated levels of total cholesterol, triglyceride, LDL, VLDL, MPO, SOD, TNF-α, IL-1β, and IL-6.
- AU activated key signaling pathways including Nrf2, PPARs, AMPK, and AKT, promoting beneficial cellular responses.
Conclusions:
- Aucubin (AU) exhibits hypolipidemic effects through potent anti-inflammatory and antioxidant activities.
- AU demonstrates potential as a novel therapeutic candidate for targeting non-alcoholic fatty liver disease (NAFLD).
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