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.

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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