Haiying Huang1, Luoyang Tu1. 1. Department of Critical Care Medicine, Sir Run Run Shaw Hospital Affiliated School of Medicine, Zhejiang University 3 East Qingchun Rd. Jianggan District, Hangzhou, Zhejiang Province, People's Republic of China.
Abstract
OBJECTIVE: This study aims to study the expression changes of S100 family proteins in neonatal rats with sepsis and investigate the effect and significance of S100 family proteins in pathogenesis and development of sepsis. METHODS: The functions of S100 family proteins were analyzed with bioinformatics. The immune-associated proteins were chosen as the candidate proteins. Twenty neonatal SPF SD rats were randomly divided into two groups: sepsis model group and control group. The liver sample was stained with HE to evaluate the establishment of sepsis model. The expression amount of proinflammatory factor IL-1, IL-6 and TNF-α was detected with ELISA. The expression changes of S100A8, S100A9, S100A11 and S100A12 in sepsis model rats were detected with real-time PCR and Western blotting. After shRNA plasmid was transfected into THP-1 cells and the expression of S100A12 was silenced, the expression changes of proinflammatory factor IL-1, IL-6 and TNF-α in LPS-induced inflammation were studied in order to investigate the S100A12 mediated inflammatory process. RESULTS: IL-1, IL-6 and TNF-α in the serum of rats with sepsis induced by LPS were 55.79 ± 3.80 ng/l, 48.76 ± 1.03 ng/l and 29.98 ± 2.27 ng/l respectively. S100A8, S100A9, S100A11 and S100A12 detected with real-time PCR in sepsis model group were 14.4 ± 1.37, 10.23 ± 1.81, 5.5 ± 1.64 and 9.97 ± 1.82 respectively. Compared with the control group, S100A8, S100A9, and S100A12 were significantly up-regulated. The shRNA silenced the expression of S100A12 which reduced the expression of proinflammatory factors after LPS stimulated the cells (P < 0.05). CONCLUSION: Compared with the control group, S100A8, S100A9, and S100A12 were significantly up-regulated in rat sepsis model group. After the expression of S100A12 in propylene glycol monomethyl ether acetate (PMA) induced human macrophages was silenced, the expression of proinflammatory factor IL-1, IL-6 and TNF-α was down-regulated.
OBJECTIVE: This study aims to study the expression changes of S100 family proteins in neonatal rats with sepsis and investigate the effect and significance of S100 family proteins in pathogenesis and development of sepsis. METHODS: The functions of S100 family proteins were analyzed with bioinformatics. The immune-associated proteins were chosen as the candidate proteins. Twenty neonatal SPF SD rats were randomly divided into two groups: sepsis model group and control group. The liver sample was stained with HE to evaluate the establishment of sepsis model. The expression amount of proinflammatory factor IL-1, IL-6 and TNF-α was detected with ELISA. The expression changes of S100A8, S100A9, S100A11 and S100A12 in sepsis model rats were detected with real-time PCR and Western blotting. After shRNA plasmid was transfected into THP-1 cells and the expression of S100A12 was silenced, the expression changes of proinflammatory factor IL-1, IL-6 and TNF-α in LPS-induced inflammation were studied in order to investigate the S100A12 mediated inflammatory process. RESULTS:IL-1, IL-6 and TNF-α in the serum of rats with sepsis induced by LPS were 55.79 ± 3.80 ng/l, 48.76 ± 1.03 ng/l and 29.98 ± 2.27 ng/l respectively. S100A8, S100A9, S100A11 and S100A12 detected with real-time PCR in sepsis model group were 14.4 ± 1.37, 10.23 ± 1.81, 5.5 ± 1.64 and 9.97 ± 1.82 respectively. Compared with the control group, S100A8, S100A9, and S100A12 were significantly up-regulated. The shRNA silenced the expression of S100A12 which reduced the expression of proinflammatory factors after LPS stimulated the cells (P < 0.05). CONCLUSION: Compared with the control group, S100A8, S100A9, and S100A12 were significantly up-regulated in ratsepsis model group. After the expression of S100A12 in propylene glycol monomethyl ether acetate (PMA) induced human macrophages was silenced, the expression of proinflammatory factor IL-1, IL-6 and TNF-α was down-regulated.
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