Protective Effects of Phytic Acid on CCl4-Induced Liver Fibrosis in Mice

Author:

Xu Zhen1ORCID,Chen Zhao1ORCID,Lan Tongtong1ORCID,Han Yisa1ORCID,Yang Ning1ORCID,Wang Chuhui1ORCID,Tao Meng1ORCID,Li Hui1ORCID,Song Yang1ORCID,Ma Xuezhen2ORCID

Affiliation:

1. Department of Nutrition and Food Hygiene, School of Public Health, College of Medicine, Qingdao University, Qingdao, China

2. The Affiliated Qingdao Central Hospital of Qingdao University, The Second Affiliated Hospital of Medical College of Qingdao University, Qingdao, China

Abstract

Liver fibrosis is the main pathological feature of various chronic liver diseases that can progress to cirrhosis. However, no effective treatment strategy for liver fibrosis is available. Phytic acid (PA) is a natural plant compound found in cereals, legumes, and rapeseed. Currently, there are few reports on its relationship with liver fibrosis. Herein, we explored the effects of PA on liver fibrosis. In this study, the liver fibrosis model was constructed by intraperitoneal injection of CCl4 and intragastric administration of sodium phytate (100 mg/kg) or silymarin (100 mg/kg) five times a week. The CCl4 injection could significantly increase the content of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and induce the damage of liver cells, infiltration of inflammatory factors, and deposition of collagen fibers in the liver tissue. Compared to the CCl4 group, PA significantly reduced AST and ALT. Also, PA alleviated liver damage and reduced inflammatory cell infiltration, collagen deposition area, and hydroxyproline (Hyp) content in the liver tissue, as well as downregulated α-smooth muscle actin (α-SMA) and collagen I (Col-1). Mechanistically, PA downregulated PI3K, p-AKT, p-p65, and p-IκBα in the liver tissue and reduced the release of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). In conclusion, PA might ameliorate liver fibrosis by inhibiting the NF-κB and PI3K/AKT signaling pathways.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Pharmacology,Food Science,Biophysics

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