Related Experiment Video
Updated: Apr 29, 2026
Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity
Published on: March 16, 2018
Asperosaponin VI Alleviates Cisplatin-Induced Liver Injury Through the Nrf2/HO-1 Signaling Pathway
Han-Hua Li1,2, Xiao-Ming Zhou3, Chuan-Wei Sun2
1Department of Gastrointestinal Surgery, Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Background:
Cisplatin (Cis) chemotherapy-induced hepatotoxicity frequently leads to treatment interruption or dose reduction, ultimately compromising therapeutic outcomes. Asperosaponin VI (AVI), a bioactive triterpenoid saponin extracted from Dipsacus asperoides, has demonstrated anti-inflammatory and antioxidant properties in various pathological conditions. However, its hepatoprotective efficacy against cisplatin-induced hepatotoxicity and underlying molecular mechanisms remain poorly understood.
Methods:
This study utilized both in vitro (LO2 human hepatocytes) and in vivo (C57BL/6mice n = 4 per group) experimental approaches to investigate the protective effects of AVI against cisplatin-induced acute hepatotoxicity. Cell viability was assessed using CCK-8 assay, while hepatic injury was evaluated through histopathological examination, biochemical markers (ALT, AST, GSH), and TUNEL staining. The involvement of the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway was confirmed using Brusatol, a specific Nrf2 inhibitor.
Results:
AVI (400 μM in vitro; 20 mg/kg in vivo) significantly attenuated cisplatin-induced cytotoxicity in LO2cells and reduced hepatic injury in mice. Treatment with AVI markedly decreased serum transaminase levels (ALT: 68.3 ± 30.4 vs. 358.1 ± 67.5 U/L, p < 0.001; AST: 129.0 ± 45.9 vs. 374.4 ± 49.5 U/L, p < 0.001), ameliorated oxidative stress, and suppressed inflammatory responses. AVI significantly upregulated Nrf2and HO-1 protein expressions while downregulating pro-inflammatory mediators (TNF-α, IL-1β, IL-6) and apoptotic markers (Caspase-1, Caspase-3, NLRP3). Pharmacological inhibition of Nrf2 with Brusatol abolished the protective effects of AVI.
Conclusions:
AVI effectively protects against cisplatin-induced hepatotoxicity through activation of the Nrf2/HO-1 signaling pathway, suggesting its potential as a novel hepatoprotective agent in cisplatin-based chemotherapy.
