scholarly journals Effective Prevention of Liver Fibrosis by Liver-targeted Hydrodynamic Gene Delivery of Matrix Metalloproteinase-13 in a Rat Liver Fibrosis Model

2016 ◽  
Vol 5 ◽  
pp. e276 ◽  
Author(s):  
Hiroyuki Abe ◽  
Kenya Kamimura ◽  
Yuji Kobayashi ◽  
Masato Ohtsuka ◽  
Hiromi Miura ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Gene Delivery ◽  
Matrix Metalloproteinase ◽  
Rat Liver ◽  
Effective Prevention ◽  
Matrix Metalloproteinase 13 ◽  
Rat Liver Fibrosis

Dahuang Zhechong pill attenuates CCl4‐induced rat liver fibrosis via the PI3K‐Akt signaling pathway

2019 ◽  
Vol 121 (2) ◽  
pp. 1431-1440 ◽  
Author(s):  
Zhenghua Gong ◽  
Jiayu Lin ◽  
Jie Zheng ◽  
Liya Wei ◽  
Li Liu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Rat Liver ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Rat Liver Fibrosis

scholarly journals The Use of Antifibrotic Recombinant nAG Protein in a Rat Liver Fibrosis Model

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Maha M. Arafah ◽  
Mohammad M. Al-Qattan ◽  
Durria A. Abdulmaged-Ahmed ◽  
Ghada A. Al-Nafesah ◽  
Nessrin Y. Jadu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Rat Liver ◽  
Serum Levels ◽  
Senior Author ◽  
Control Group ◽  
Protein Markers ◽  
Group Iii ◽  
Group I ◽  
Cord Injury ◽  
Rat Liver Fibrosis

Objectives. The “nAG” protein is the key protein mediating the regeneration of amputated limbs in salamanders. The senior author (MMA) developed the original hypothesis that since “nAG” is a “regenerative” protein, it must be also an “antifibrotic’ protein. The antifibrotic properties were later confirmed in a rabbit skin hypertrophic scar model as well as in a rat spinal cord injury model. The aim of this study is to evaluate the potential therapeutic properties of the nAG protein in a rat liver fibrosis model. Methodology. Liver fibrosis was induced using intraperitoneal injections of carbon tetrachloride (CCL4). A total of 45 rats were divided equally into 3 groups: Group I (the control group) received normal saline injections for 8 weeks, Group II received CCL4 for 8 weeks, and Group III received CCL4 and nAG for 8 weeks. At the end of the experiment, the serum levels of 6 proteins (hyaluronic acid, PDGF-AB, TIMP-1, laminin, procollagen III N-terminal peptide, and collagen IV-alpha 1 chain) were measured. Liver biopsies were also taken and the stages of live fibrosis were assessed histologically. Results. The CCL4 treatment resulted in a significant increase in the serum levels of all 6 measured proteins. The nAG treatment significantly reduced these high levels. The degree of liver fibrosis was also significantly reduced in the CCL4/nAG group compared to the CCL4 group. Conclusions. nAG treatment was able to significantly reduce the serum levels of several protein markers of liver fibrosis and also significantly reduced the histological degree of liver fibrosis.

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