Abstract
In this study, purification, preliminary characterization and hepatoprotective effects of water-soluble polysaccharides from dandelion root (DRP) were investigated. Two polysaccharides, DRP1 and DRP2, were isolated from DRP. The two polysaccharides were α-type polysaccharides and didn’t contain protein. DRP1, with a molecular weight of 5695 Da, was composed of glucose, galactose and arabinose, whereas DRP2, with molecular weight of 8882 Da, was composed of rhamnose, galacturonic acid, glucose, galactose and arabinose. The backbone of DRP1 was mainly composed of (1→6)-linked-α-d-Glc and (1→3,4)-linked-α-d-Glc. DRP2 was mainly composed of (1→)-linked-α-d-Ara and (1→)-linked-α-d-Glc. A proof-of-concept study was performed to assess the therapeutic potential of DRP1 and DRP2 in a mouse model that mimics acetaminophen (APAP) -induced liver injury (AILI) in humans. The present study shows DRP1 and DRP2 could protect the liver from APAP-induced hepatic injury by activating the Nrf2-Keap1 pathway. These conclusions demonstrate that the DRP1 and DRP2 might be suitable as functional foods and natural drugs in preventing APAP-induced liver injury.
Highlights
Acetaminophen (APAP), a commonly used over-the-counter antipyretic and analgesic, is safe in therapeutic doses, overdoses may cause acute liver injury
DRP1 and DRP2 accounted for 70.4% and 22.8% of the total dandelion root polysaccharide (DRP) content, respectively
Histopathological analysis of liver tissues indicated significantly reduced areas of necrosis in mice after treatment with DRP1 and DRP2 compared with the APAP-alone group. These results indicated the protective effects of DRP1 and DRP2 against APAP-induced liver injury
Summary
Acetaminophen (APAP), a commonly used over-the-counter antipyretic and analgesic, is safe in therapeutic doses, overdoses may cause acute liver injury. Most APAP is metabolized by sulfation and glucuronidation, and only a small fraction is oxidized by the cytochrome P450 system, resulting in the formation of a highly reactive intermediate metabolite called. When over-dosed, NAPQI deplete hepatic glutathione and bind covalently to intracellular proteins, resulting in increased oxidative stress and hepatic necrosis [1,2]. In response to oxidative stress, cytoprotective enzymes were activated in the liver mounts. 2 (Nrf2), which is a key factor that plays a central role in cellular defense against oxidative and electrophilic insults. Nrf is a transcription factor that regulates the expression of various cytoprotective enzymes by binding to the antioxidant response element (ARE) domain upstream of their promoter
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