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| Effects of Kupffer cell inactivation on graft survival and liver regeneration after partial liver transplantation in rats |
| Hang-Yu Luo, Shan-Fang Ma, Ji-Fu Qu and De-Hu Tian |
Beijing, China
Author Affiliations: Department of Emergency Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China (Luo HY and Ma SF); Department of Emergency Medicine, Daping Hospital, Third Military Medical University, Chongqing 400042, China (Qu JF); Orthopetics Department, Third Hospital of Hebei Medical University, Shijiazhuang 050051, China (Tian DH)
Corresponding Author: Shan-Fang Ma, MD, Department of Emergency Medicine, Beijing Ditan Hospital, Capital Medical University, 8 Jingshun East Street, Chaoyang District, Beijing 100015, China (Tel: +86-10- 84322120; Fax: +86-10-84322999; Email: enever@live.cn) |
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Abstract BACKGROUND: Gadolinium chloride (GdCl3) selectively inactivates Kupffer cells and protects against ischemia/reperfusion and endotoxin injury. However, the effect of Kupffer cell inactivation on liver regeneration after partial liver transplantation (PLTx) is not clear. This study was to investigate the role of GdCl3 pretreatment in graft function after PLTx, and to explore the potential mechanism involved in this process.
METHODS: PLTx (30% partial liver transplantation) was performed using Kamada's cuff technique, without hepatic artery reconstruction. Rats were randomly divided into the control low-dose (5 mg/kg) and high-dose (10 mg/kg) GdCl3 groups. Liver injury was determined by the plasma levels of alanine aminotransferase and aspartate aminotransferase, liver regeneration by PCNA staining and BrdU uptake, apoptosis by TUNEL assay. IL-6 and p-STAT3 levels were measured by ELISA and Western blotting.
RESULTS: GdCl3 depleted Kupffer cells and decreased animal survival rates, but did not significantly affect alanine aminotransferase and aspartate aminotransferase (P>0.05). GdCl3 pretreatment induced apoptosis and inhibited IL-6 overexpression and STAT3 phosphorylation after PLTx in graft tissues.
CONCLUSION: Kupffer cells may contribute to the liver regeneration after PLTx through inhibition of apoptosis and activation of the IL-6/p-STAT3 signal pathway.
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2015, Vol. 14 
