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Exploring Plasma Protein C and Inflammatory Pathways in Bile Duct Ligation‐Induced Liver Fibrosis in Rats
Author(s) -
Saha Joy K,
Engle Steven K,
Xia Jinqi,
Sandusky George E,
Gerlitz Bruce,
Grinnell Brian,
Jakubowski Joseph A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a808
Subject(s) - fibrosis , albumin , chemokine , inflammation , medicine , pathology , hepatic fibrosis
The present study characterized the induction of liver fibrosis and elaboration of biomarkers during progression of liver fibrosis induced by bile duct ligation (BDL) in rats. Following BDL, the severity of liver damage progressed in a time‐dependent manner as assessed by an increase in bridging fibrosis, a hallmark of human liver fibrosis. Plasma protein C, albumin, and total protein levels were significantly decreased, whereas serum sICAM‐1 and TIMP‐1 levels were significantly increased along with fibrogenesis. Serum biochemical markers of liver function as well as circulating neutrophils, monocytes, RBCs, and platelets, significantly increased with progression of liver fibrosis. Inflammatory chemokines and cytokines were also significantly increased with progression of disease severity. The differential changes in GGT, HA, sICAM‐1, neutrophils and several inflammatory chemokines suggest the involvement of inflammatory pathways in BDL‐induced liver fibrosis. In summary, plasma protein C, along with several other noninvasive biochemical parameters, correlated significantly with severity of liver histopathology and may serve as potential biomarkers in liver fibrosis.