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Related Experiment Videos

Notoginsenoside R1 Alleviates Acetaminophen-Induced Liver Injury via MAPK/mTOR-Mediated Autophagy.

Shuangjiang Li1,2,3, Zhipeng Liu1,2,3, Guandong Pan4,5

  • 1Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi, Medical University, Nanning, Guangxi 530021, China.

The American Journal of Chinese Medicine
|July 16, 2026
PubMed
Summary

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Notoginsenoside R1 (NGR1) effectively protects against acetaminophen-induced liver injury by inhibiting MAPK/mTOR signaling, promoting autophagy, and suppressing ferroptosis. This natural compound shows promise as a therapeutic for acute liver failure.

Area of Science:

  • Hepatology
  • Pharmacology
  • Natural Product Chemistry

Background:

  • Acetaminophen overdose is a primary cause of acute liver injury (ALI), with limited therapeutic options.
  • Notoginsenoside R1 (NGR1), a saponin from Panax notoginseng, possesses anti-inflammatory and antioxidant properties.
  • The hepatoprotective effects and mechanisms of NGR1 in acetaminophen-induced liver injury (AILI) require systematic investigation.

Purpose of the Study:

  • To evaluate the hepatoprotective potential of NGR1 against AILI in a mouse model.
  • To elucidate the underlying molecular mechanisms, including the involvement of the MAPK/mTOR-autophagy pathway.

Main Methods:

  • Established an AILI mouse model.
  • Assessed NGR1's effects using biochemical assays, histopathology, Western blotting, and immunofluorescence.
Keywords:
APAPAcute Liver InjuryAutophagyMAPK/mTORNotoginsenoside R1

Related Experiment Videos

  • Employed integrative transcriptomic, metabolomic, and gut microbiota analyses; validated mechanisms with L-leucine (mTOR activator).

    • Main Results:

    • NGR1 significantly attenuated AILI, reducing liver enzymes (ALT/AST), improving histology, and increasing survival.
    • NGR1 suppressed inflammation and oxidative stress by modulating key cytokines and antioxidant/oxidative markers.
    • Multi-omics revealed NGR1's impact on MAPK/mTOR signaling, autophagy, ferroptosis, and glutathione metabolism.

    Conclusions:

    • NGR1 protects against AILI by inhibiting MAPK/mTOR signaling, promoting autophagy, and suppressing ferroptosis.
    • NGR1 demonstrates significant therapeutic potential for acetaminophen-induced hepatotoxicity.
    • Further research into NGR1 as a clinical candidate for acute liver injury is warranted.