›› 2014, Vol. 29 ›› Issue (8): 838-842.DOI: 10.3969/j.issn.1673-8640.2014.08.013

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The expression and significance of extracellular ATP in murine acute liver injury model

HU Meicong1, ZOU Lingli2, HUANG Baojun3, WANG Lei   

  1. 1. Department of Laboratory Medicine, Zhejiang Medical College, Zhejiang Hangzhou 310053, China;
    2. Haiqin Zone,Hangzhou Sanatorium of Nanjing Military Region,Zhejiang Hangzhou 310002,China;
    3. Department of Immunology, Anhui Medical University, Anhui Hefei 230032, China
  • Received:2013-11-24 Online:2014-08-30 Published:2014-09-05

Abstract: Objective To observe the expression and significance of extracellular adenosine triphosphate (eATP) in concanavalin A (ConA)-induced murine acute liver injury model. Methods A total of 72 mice were randomly classified into control group (saline, 36 cases) and ConA group (20 mg/kg ConA, 36 cases). The blood specimens and liver tissues were collected at 2, 6, 12, 18, 24 and 48 h after injection. The activities of serum alanine aminotransferase (ALT) were measured by Reitman Frankel assay. Hematoxylin-eosin (HE) dyeing was carried out to assess the pathological change of liver tissue. The levels of eATP in serum were detected by chemiluminescence. Western-blot was employed to detect the expression of purinoceptor P2(P2X7). The contents of serum interleukin 1 beta (IL-1β) were assayed by enzyme-linked immunosorbent assay (ELISA). Results The ConA-induced murine acute liver injury model was constructed successfully. The level of eATP increased at 2 h after ConA injection, and reached peak at 18 h (700 nmol / L). Meanwhile, there expressed P2X7 in liver tissues. Compared with control group, the IL-1β levels in serum of ConA group increased significantly (P<0.01). Conclusions In ConA-induced murine acute liver injury model, eATP releases from the injury liver tissues, and might influence the synthesis and secretion of inflammatory cytokine IL-1β through the P2X7 pathway, eventually aggravating the process of acute liver injury.

Key words: Adenosine triphosphate, Concanavalin A, Liver injury, Inflammasome, Interleukin 1beta

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