Low-Molecular-Weight Oligonol, a Polyphenol Derived from Lychee Fruit, Attenuates Experimental Reflux Esophagitis and HCl/Ethanol-Induced Gastric Ulcer.

Oligonol, a polyphenol derived from lychee fruit, is produced by an oligomerization process that converts high-molecular-weight polyphenol polymers into low-molecular-weight oligomers. Evidence suggests that oligonol exerts its beneficial effects based on antioxidant and anti-inflammatory properties. This study was the first to investigate the antioxidative and anti-inflammatory effects of oligonol on gastroesophageal inflammatory models: surgically induced acute reflux esophagitis (RE) and gastric ulcer (GU) induced by HCl/ethanol. In the in vitro study, 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazolin-6-sulfonic acid) (ABTS) radical scavenging assays were performed to determine the antioxidant activity of oligonol. The experimental groups were each composed of normal, vehicle, and oligonol groups. RE rats and GU mice were treated orally with oligonol (100 mg/kg bw) or distilled water as a vehicle (n = 8 for each group). Oligonol exhibited potent free radical-scavenging capacities for DPPH and ABTS radicals, activities that were similar to those of ascorbic acid. The in vivo study revealed that oligonol consumption significantly prevented RE and GU formation and decreased the gross mucosal injury from oxidative stress. Oligonol decreased the reactive oxygen species levels and elevated levels of both inflammatory mediators and cytokines (p-IκB, NF-κBp65, COX-2, iNOS, TNF-α, and IL-1ß) in the RE and GU models. Oligonol had a protective effect against oxidative stress by regulating antioxidant enzyme (superoxide dismutase, catalase, and GPx-1/2) activities in GU mice. Oligonol has potential as a preventive and therapeutic agent for gastroesophageal inflammatory diseases, including RE and GU.

Chondroitin Sulfate-Rich Extract of Skate Cartilage Attenuates Lipopolysaccharide-Induced Liver Damage in Mice.

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.