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The protective role of Hepatopoietin Cn on liver injury induced by carbon tetrachloride in rats *
Author(s) -
Cui ChunPing,
Wei Ping,
Liu Yang,
Zhang DaJin,
Wang LiSheng,
Wu ChuTse
Publication year - 2009
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2008.00447.x
Subject(s) - carbon tetrachloride , ccl4 , liver injury , hepatocyte , hydroxyproline , in vivo , immunostaining , intraperitoneal injection , fibrosis , chemistry , alanine transaminase , hepatic fibrosis , medicine , endocrinology , pharmacology , in vitro , immunohistochemistry , biology , biochemistry , microbiology and biotechnology , organic chemistry
Background: Hepatopoietin Cn (HPPCn) is a member of the leucine‐rich acidic nuclear protein family (LANP), and studies of partially hepatectomized (PH) mice show that levels of HPPCn mRNA increase following liver injury. Furthermore, the recombinant human protein (rhHPPCn) was shown to stimulate hepatic DNA synthesis and activate signaling pathways involved in hepatocyte proliferation in vitro and in vivo . Aim: The aim of the study was to evaluate the protective effect of rhHPPCn on liver injury and fibrosis induced by carbon tetrachloride (CCl4) injection. Methods: Wistar rats weighing 200 g were given a single and repeated intraperitoneal injections of CCl4. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity in rat serum were measured using biochemical assay. Hepatic hydroxyproline (Hyp) level was determined in the hydrolysates of liver samples. Immunostaining and Masson's trichrome staining were conducted to evaluate hepatocyte proliferation and fibrosis. Results: The results showed that exogenous rhHPPCn could alleviate hepatocyte necrosis and protect the liver from the development of fibrotic lesions by proliferation stimulation. Additionally, HPPCn could reduce ALT/AST levels in rat serum following single and repeated CCl4 injection. Conclusion: It was suggested that HPPCn could protect hepatocytes from injury induced by CCl4 as a proliferation stimulator.