Abstract
The late stages of liver fibrosis are considered to be irreversible. Red quinoa (Chenopodium formosanum Koidz), a traditional food for Taiwanese aborigines, was gradually developed as a novel supplemental food due to high dietary fibre and polyphenolic compounds. Its bran was usually regarded as the agricultural waste, but it contained a high concentration of rutin known as an antioxidant and anti-inflammatory agent. This study is to explore the effect of red quinoa bran extracts on the prevention of carbon tetrachloride (CCl4)-induced liver fibrosis. BALB/c mice were intraperitoneally injected CCl4 to induce liver fibrosis and treated with red quinoa whole seed powder, bran ethanol extracts, bran water extracts, and rutin. In the results, red quinoa powder provided more protection than rutin against CCl4-induced oxidative stress, pro-inflammatory factor expression and fibrosis development. However, the bran ethanol extract with high rutin content provided the most liver protection and anti-fibrosis effect via blocking the tumor necrosis factor alpha (TNF-α)/interleukin 6 (IL-6) pathway and transforming growth factor beta 1 (TGF-β1) pathway.
Highlights
Liver injury is caused by hepatic virus infection, alcohol abuse, medicine, toxin, abnormal food consumption, metabolic syndrome and other factors
The CCL group had significantly higher liver weight than the NOR group (p < 0.05) but the CCL group had significantly lower final body weight than the NOR group (p < 0.05). This result indicated that the relative liver to body weight in the CCL group was significantly higher than in the NOR group (p < 0.05)
The HL-E and HL-W group had significantly higher relative liver to body weight compared to the CCL group (p < 0.05)
Summary
Liver injury is caused by hepatic virus infection, alcohol abuse, medicine, toxin, abnormal food consumption, metabolic syndrome and other factors. Chronic liver injury can result in liver fibrosis, cirrhosis, liver malfunction and hepatocellular carcinoma [1]. T cells, which secretes pro-inflammatory cytokines, such as interleukin 6 (IL-6) [2]. A repeated liver injury and wound healing response will lead to liver fibrosis and cirrhosis. T cells and macrophages secrete tumour necrosis factor alpha (TNF-α), IL-6 and transforming growth factor beta. TGF-β1 mediates activation of hepatic satellites cells (HSCs), which transforms the tissue-resident fibroblasts into activated myofibroblasts
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