Abstract
The protective effects of a chondroitin sulfate-rich extract (CSE) from skate cartilage against lipopolysaccharide (LPS)-induced hepatic damage were investigated, and its mechanism of action was compared with that of chondroitin sulfate (CS) from shark cartilage. ICR mice were orally administrated 200 mg/kg body weight (BW) of CS or 400 mg/kg BW of CSE for 3 consecutive days, followed by a one-time intraperitoneal injection of LPS (20 mg/kg BW). The experimental groups were vehicle treatment without LPS injection (NC group), vehicle treatment with LPS injection (LPS group), CS pretreatment with LPS injection (CS group), and CSE pretreatment with LPS injection (CSE group). Hepatic antioxidant enzyme expression levels in the CS and CSE groups were increased relative to those in the LPS group. In LPS-insulted hepatic tissue, inflammatory factors were augmented relative to those in the NC group, but were significantly suppressed by pretreatment with CS or CSE. Moreover, CS and CSE alleviated the LPS-induced apoptotic factors and mitogen-activated protein kinase (MAPK). In addition, CS and CSE effectively decreased the serum lipid concentrations and downregulated hepatic sterol regulatory element-binding proteins expression. In conclusion, the skate CSE could protect against LPS-induced hepatic dyslipidemia, oxidative stress, inflammation, and apoptosis, probably through the regulation of MAPK signaling.
Highlights
Chondroitin sulfate (CS) is a glycosaminoglycan that is present in the extracellular matrix of animal tissue, especially in cartilages, skin, blood vessels, ligaments, and tendons, where it forms an essential component of proteoglycans (Figure 1) [1,2]
LPSbody treatment significantly decreased the liver(37.7–38.0 weight in groupThere relative significantly less body weight changes during days in the groups than in the in the NC group, whereas chondroitin sulfate (CS) and chondroitin sulfate-rich extract (CSE) treatments effectively protected against the reduction of liver group (p < 0.05)
We investigated the inhibitory effect of skate CSEs on proinflammatory and and apoptotic mediators, and explored the possible mechanism of action of the compound in the apoptotic mediators, and explored the possible mechanism of action of the compound in the liver of liver of LPS‐injected mice
Summary
Chondroitin sulfate (CS) is a glycosaminoglycan that is present in the extracellular matrix of animal tissue, especially in cartilages, skin, blood vessels, ligaments, and tendons, where it forms an essential component of proteoglycans (Figure 1) [1,2]. CS plays an important role in the elasticity and function of articular cartilage. In addition to these structural properties, CS exhibits a wide variety of biological functions due mainly to the presence of rare oversulfated building units in its domain structure that interact with other molecules [3]. CS is currently recommended by the European League Against Rheumatism as a SYSADOA Mar. Drugs 2017, 15, 178; doi:10.3390/md15060178 www.mdpi.com/journal/marinedrugs.
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