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Heat shock protein 47 as indispensible participant in liver fibrosis: Possible protective effect of lactoferrin
Author(s) -
Rizk Fatma H.,
Sarhan Naglaa I.,
Soliman Nema A.,
Ibrahim Marwa A. A.,
AbdElsalam Marwa,
AbdElsalam Sherief
Publication year - 2018
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1884
Subject(s) - lactoferrin , heat shock protein , shock (circulatory) , liver fibrosis , chemistry , fibrosis , medicine , biochemistry , gene
Lactoferrin (LF) was previously suggested to have a protective effect against liver fibrosis by preventing hepatic stellate cells (HSCs) activation. The effect of LF on heat shock protein 47 (HSP47) has not yet been studied so this study was designed to investigate LF effect on HSP47 as a potential target for management of liver fibrosis and comparing it with silymarin (SM) in a thioacetamide (TAA)‐induced liver fibrosis model. Rats were divided into four groups; normal control, TAA (TAA‐treated), LF (LF + TAA‐treated), and SM (SM + TAA‐treated). After 6 weeks, both LF and SM improved the grade of cirrhosis, reduced collagen fibers deposition, inactivated HSCs, significantly decreased elevated liver enzymes, HSP47, hydroxyproline content, transforming growth factor‐beta 1, matrix metalloproteinase‐2, 8‐hydroxydeoxyguanosine, malondialdehyde, nitric oxide levels and the percentage of alpha smooth muscle actin positive HSCs compared with TAA group. Moreover, LF significantly increased the total antioxidant capacity compared with TAA group. It could be concluded that LF is a promising antifibrotic drug and could be considered as one of the HSP47 inhibitors but SM is still more potent. © 2018 IUBMB Life, 70(8):795–805, 2018