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Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice
Chun-Mei Li1,2,3,4, Tian Sun1,2,3,4, Mou-Jie Yang1,2
1Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, the Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi Zhuang Autonomous Region, China.
Background:
Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.
Aim:
To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.
Methods:
A model of APAP-induced liver injury was used to study the protective effect of C2-FH on liver injury. C2-FH was administered through intraperitoneal injection 30 minutes after APAP treatment. We detected the effects of C2-FH on liver function, inflammatory response and complement activation. Additionally, RNA-sequencing (RNA-Seq) analysis was conducted to understand the mechanism through which C2-FH provides protection against APAP-induced liver injury.
Results:
C2-FH inhibited the increase in serum alanine aminotransferase activity, aspartate aminotransferase activity and lactate dehydrogenase, and reduced liver tissue necrosis caused by APAP. Moreover, it attenuated the inflammatory response and inhibited complement activation in APAP-induced liver injury. RNA-Seq analysis provided additional explanations for the protective role of C2-FH against APAP-induced liver injury.
Conclusion:
C2-FH attenuates APAP-induced liver injury by inhibiting complement activation.
Insights
Complement inhibitor C2-FH protects the liver from acetaminophen (APAP) damage by reducing inflammation and inhibiting complement activation, offering a potential therapeutic strategy for APAP-induced liver injury.
Area of Science:
- Immunology
- Hepatology
- Pharmacology
Background:
- Complement activation significantly contributes to acetaminophen (APAP)-induced liver injury.
- The specific role of the complement inhibitor C2-FH in mitigating this damage was previously unknown.
Purpose of the Study:
- To investigate the protective effects of C2-FH against APAP-induced liver injury.
- To determine if C2-FH functions by inhibiting complement activation.
Main Methods:
- APAP-induced liver injury model in mice.
- Intraperitoneal administration of C2-FH post-APAP treatment.
- Assessment of liver function markers, inflammatory responses, and complement activation.
- RNA-sequencing (RNA-Seq) analysis to elucidate protective mechanisms.
Main Results:
- C2-FH administration significantly reduced liver injury markers (ALT, AST, LDH) and liver necrosis.
- C2-FH effectively attenuated inflammatory responses and suppressed complement activation.
- RNA-Seq analysis provided mechanistic insights into C2-FH's protective actions.
Conclusions:
- C2-FH demonstrates a protective effect against APAP-induced liver injury.
- Inhibition of complement activation is a key mechanism by which C2-FH exerts its hepatoprotective effects.
