Protective effects of splenectomy of small-for-size syndrome in rat models / 中华器官移植杂志

ABSTRACT

Objective To explore the role of splenectomy in the prevention and treatment of small-for-size liver in rat models, as well as its pathophysiologic mechanism in the development of a small-for-size syndrome (SFSS). Methods The models of sham-operation and 80 % partial hepatectomy (PH) were used in rats. In the experiment group splenectomy was performed following 80% PH. The concentrations of serum tumor necrosis factor (TNF-α), the content of NF-cB p65 in liver nuclear extracts, the expression of TNF-α, intercellular adhesion molecular (ICAM-1), and proliferating cell nuclear antigen (PCNA) transcripts, the activities of serum aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), total bilirubin (TB), albumin (Alb) cholinesterase (CHE), and liver myeloperoxidase (MPO) were analyzed. Portal venous pressures (PVP),incidence of SFSS,and one-wk survival rate were measured. Results In the control rats,The PVP was obviously elevated immediately after PH. The level of NF-κB p65 was obviously increased at the first h and peaked at about 3rd h postoperatively. The transcription of TNF-α and ICAM-1 and the release of serum TNF-α were significantly increased 3 h after PH. Capillary endothelial cells of the livers strongly expressed ICAM-1 24 h after PH. Splenectomy significantly reduced the PVP and the content of NF-κB p65 in the livers in concurrence with the expression of TNF-α and ICAM-1 gene as well as the activity of MPO at the corresponding time points after PH (P＜0. 05), while increased the expression of PCNA gene (P＜0. 05). Administration of splenectomy resulted in a statistically significant decrease in AST, ALT, LDH, TB, the incidence of SFSS and increase in one-wk survival rate (P ＜ 0.05 ). Conclusion Splenectomy alleviates liver injury and promotes liver regeneration in small-for-size liver rats by reducing portal vein perfusion and pressure,and suppressing NFκB activation and subsequent expression of proinflammatory mediators.