Critical care
Can a flavonoid rescue acetaminophen livers via GPX4?
Open access · cc by · source: Europe PMC
In C57BL/6 mice, Thonningianin A (20–40 mg/kg) before APAP 300 mg/kg cut ALT/AST and ER-stress markers, but AAV8 liver GPX4 knockdown (53.6% protein loss) abolished protection.
Study at a glance
- Design
- Animal / in-vitro — C57BL/6 mice, oral Thonningianin A 20/40 mg/kg then APAP 300 mg/kg; AAV8 hepatocyte GPX4 shRNA knockdown
- N
- N=8 · Biochemistry figures report mean ± SD, n = 5–8 mice per group
- Population
- 8-week C57BL/6 mice with or without liver-targeted AAV8-GPX4 shRNA, plus APAP hepatotoxicity
- Outcome
- Plasma ALT/AST, hepatic cytokines/oxidative-stress markers, apoptosis and ER-stress proteins, dependence on GPX4
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Key findings
TA lowered ALT/AST, IL-1β/IL-6/TNF-α/MCP-1, raised BCL-2, and cut CHOP/BAX, GRP78, p-PERK, and ATF4. GPX4 knockdown (53.6% protein drop) raised ALT/AST again despite TA.
Methodology
Pretreated mice with oral TA 20 or 40 mg/kg, then i.p. APAP 300 mg/kg; measured ALT/AST, cytokines, apoptosis/ER-stress proteins, and repeated the APAP+TA experiment after hepatocyte GPX4 shRNA (AAV8).
Limitations
Mouse APAP overdose is not a registered human trial of TA; n=5–8/group cannot define a clinical dose, and GPX4 knockdown does not prove TA binds GPX4 directly.
How this study connects
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