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J Dairy Sci. 2014;97(6):3281-91. doi: 10.3168/jds.2013-7505. Epub 2014 Apr 14.

Lactoferrin protects against chemical-induced rat liver fibrosis by inhibiting stellate cell activation.

Author information

1
Department of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, Taiwan.
2
Department of Bioresources, Da-Yeh University, Changhwa 515, Taiwan.
3
Department of Physiology, National Cheng Kung University, Tainan 404, Taiwan.
4
Department of Medical Biotechnology and Laboratory Science, Chang Gung University, Tao-Yuan 333, Taiwan.
5
Department of Animal Science and Biotechnology, Tunghai University, Taichung 407, Taiwan.
6
Department of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, Taiwan; Rong Hsing Research Center for Translational Medicine, and Integrative Evolutionary Galliform Genomics Center, National Chung Hsing University, Taichung 402, Taiwan. Electronic address: chchen1@dragon.nchu.edu.tw.

Abstract

Liver diseases, which can be caused by alcohol abuse, chemical intoxication, viral hepatitis infection, and autoimmune disorders, are a significant health issue because they can develop into liver fibrosis and cirrhosis. Lactoferrin (LF), a siderophilic protein with 2 iron-binding sites, has been demonstrated to possess a multitude of biological functions, including antiinflammation, anticancer, and antimicrobial effects, as well as immunomodulatory-enhancing functions. In the current study, we induced hepatotoxicity in rats with dimethylnitrosamine (DMN) to establish a situation that would enable us to evaluate the hepatoprotective effects of LF against hepatic injury. Our results showed that DMN-induced hepatic pathological damage significantly decreased the body weight and liver index, increased the mRNA and protein levels of collagen α-1(I) (ColIα-1) and α-smooth muscle actin, and increased the hydroxyproline content. However, treatment with LF significantly increased body weight and liver index, decreased the mRNA and protein levels of ColIα-1 and α-smooth muscle actin, and suppressed the hydroxyproline content when compared with the DMN-treated group. Liver histopathology also showed that low-dose LF (100mg/kg of body weight) or high-dose LF (300 mg/kg of body weight) could significantly reduce the incidences of liver lesions induced by DMN. These results suggest that the LF exhibits potent hepatoprotection against DMN-induced liver damage in rats and that the hepatoprotective effects of LF may be due to the inhibition of collagen production and to stellate cell activation.

KEYWORDS:

dimethylnitrosamine; hepatic stellate cells; lactoferrin; liver fibrosis

PMID:
24731632
DOI:
10.3168/jds.2013-7505
[Indexed for MEDLINE]
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