Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.

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.

[Trichloroethylene interferes with heart development of zebrafish via inhibiting Wnt signal pathway].

Objective: To investigate the molecular mechanism of trichloroethylene (TCE) cardiac developmental toxicity on zebrafish embryos and to try to provide experimental data for related intervention.

Methods: Zebrafish embryos were purchased from the National Zebrafish Resource Center. The embryos were divided into DMSO(control group), DMSO+CHIR, DMSO+XAV, TCE, TCE+CHIR and TCE+XAV groups(TCE at the concentration of 1, 10 and 100 ppb, with the DMSO as control; DMSO: Dimethyl suldoxide; CHIR: CHIR-99021, Wnt agonist; XAV: XAV-939, Wnt antagonist), 60 embryos per group.