Figure 5.

Restoration of TRIB1 induced macrophage anti-inflammatory M2 polarization to alleviate hepatic I/R injury. Lentiviral infection of macrophages was performed to overexpress TRIB1 following the manufacturer’s protocol. LV-infected BMDMs were infused back into the mice via the tail vein at 1 hr pre-operation. HE (a) and TUNEL-stained (b) tissue sections of livers. Average levels of serum ALT and AST in mice (c). Suzuki’s scores based on liver H&E-stained sections and TUNEL-positive percentages evaluated by ImageJ software (d). The macrophage polarization phenotype (CD86, CD206) (e) and inflammation-related gene expression (TNF-α, IFN-γ, IL-10, ARG-1) (f) were measured by qRT–PCR. CD206 detected by IHC in liver tissue sections post I/R (g). Data are presented as the mean ± SEM and performed by one-way analysis, P values <0.05 (two-tailed) were considered statistically significant.