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Autophagy in Triptolide-Mediated Cytotoxicity in Hepatic Cells
Yan Ming Wei1, Zhi Hua Luan2, Bi Wang Liu2
1College of Chinese Medicine and Food Engineering, Shanxi University of Chinese Medicine, Jinzhong, Shanxi, People's Republic of China.
International Journal of Toxicology
|July 26, 2019
Summary
Triptolide causes liver cell damage by inducing oxidative stress. Autophagy, a cellular process, protects against this damage, suggesting it could be a therapeutic target for triptolide hepatotoxicity.
Area of Science:
- Cell Biology
- Toxicology
- Pharmacology
Background:
- Triptolide, from *Tripterygium wilfordii*, has limited clinical use due to severe hepatotoxicity.
- Autophagy is crucial for cellular homeostasis and implicated in drug-induced liver injury.
Purpose of the Study:
- To investigate the role of autophagy in triptolide-induced hepatotoxicity using human liver cells (HL7702).
Main Methods:
- Treated HL7702 cells with triptolide.
- Assessed cell viability, lactate dehydrogenase leakage, and apoptosis.
- Measured autophagosome formation and autophagy-related protein expression (Beclin1, LC3II).
- Utilized N-acetylcysteine and autophagy inhibitors.
Main Results:
- Triptolide induced cytotoxicity, oxidative stress, and increased autophagy markers (autophagosomes, Beclin1, LC3II).
- N-acetylcysteine reversed triptolide's pro-autophagic effects.
- Autophagy suppression worsened triptolide-induced cell death and apoptosis.
Conclusions:
- Triptolide-induced oxidative stress enhances autophagic activity.
- Autophagy acts as a protective mechanism against triptolide hepatotoxicity in HL7702 cells.
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