Biomedical Research

Silent information regulator-2 (SIRT2) is a recently discovered type of dependence on nicotine amines adenine dinucleotide type III histone acetylation enzyme. However, the expression change and research of SIRT2 in macrophage remains unclear. Here in this study, we demonstrate that the regulatory effects of SIRT2 on sepsis and the feasible correlational research. BALB/c mice were used to establish Cecum ligation puncture (CLP)-induced sepsis model. At 3, 6, 12, 24, 48 and 72 h after CLP-induced, the expression of SIRT2 and MMP-9 gene were analyzed using Quantitative real time polymerase chain reaction (Q-PCR), the serum of ALT, inflammatory factor and MCP-1 levels were measured by ELISA kits, pathological changes of liver tissue was observed using HE Dyeing and Immuno-histochemical analysis, and the expressions of NF-κB p65 and p38MAPK protein were surveyed using western blotting. Firstly, the expression of SIRT2 gene and the serum of ALT level in sepsis mice were rapidly increased since 3 h operation and reached peak at 48 h after operation. Next, seep inflammatory cells was surged and the serum of TNF-α, IL-1, IL-6, IL-10 and MCP-1 were observably increased and reached peak at 6 or 12 h after operation in sepsis mice. Lastly, NF-κB p65 and phosphorylation-p38MAPK protein expression, and the MMP-9 gene expression were rapidly increased and reached peak at 12 h or 6 h, respectively, after operation in sepsis mice. Our data suggested that SIRT2 can increase inflammatory of sepsis mice through mediation of NF-κB and p38 MAPK pathway.

Author(s): Wen Yang, Yanbing Liang, Hao Tang, Fang Li, Zhibin Chen, Zhenyu Li, Jingguo Wu, Lijin Zeng, Zhongfu Ma
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