IL-1R1 deficiency impairs liver regeneration after 2/3 partial hepatectomy in aged mice.

Inflammation has a dual effect: it can protect the body and destroy tissue and cell as well. The purpose of this experiment was to determine the role of in liver regeneration (LR) after partial hepatectomy (PH) in aged mice. The wild-type (WT, n = 36) and the knockout (KO, n = 36) 24-month-old C57BL/6J mice underwent two-thirds PH; 33 WT mice underwent sham operation. Liver coefficient was calculated by liver/body weight. The mRNA and protein expressions of genes were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting methods, respectively. Compared with WT mice, liver coefficient was lower in the KO aged mice at 168 and 192 h (p = 0.039 and p = 0.027). The mRNA transcription of inflammation-related genes and cell cycle-associated genes decreased or delayed. The protein expressions of proliferation-related marker PCNA and proliferation-associated signaling pathway components JNK1, NF-κB and STAT3 reduced or retarded. There was stronger activation of proapoptotic proteins caspase-3, caspase-8 and BAX in the KO mice at different time points (p < 0.05 or p < 0.01). KO reduced inflammation and caused impaired liver regeneration after 2/3 partial hepatectomy in aged mice. Maintaining proper inflammation may contribute to regeneration after liver partly surgical resection in the elderly.