Protective Effect of Polysaccharide from Hizikia fusiformis Against Ethanol-Induced Toxicity

Hye-Jung Hwang, In-Hye Kim, and Taek-Jeong Nam1


I. Introduction


II. The Effect of Hf-PS-1 Against Ethanol-Induced

Gastric Damage in Rats


A. Preparation and effect of Hf-PS-1 in SD rats


B. Protective effect of Hf-PS-1 against ethanol-

induced oxidative stress


III. Effects of Hf-PS-1 Against Ethanol-Induced Injury to

IEC-6 Cells


A. Hf-PS-1 protects the ethanol-induced injury to

IEC-6 cells


B. Hf-PS-1 inhibits ethanol-induced damage by

downregulating JNK


IV. Conclusion




Abstract Polysaccharide extracted from Hizikia fusiformis (Hf-PS-1) exhibited protective effects against ethanol-induced peptic injury. In in vivo assay, the ethanol group exhibited decrease of total glutathione (GSH) and increase of jun N-terminal kinase (JNK) phosphorylation relative to the control group, whereas levels were significantly increased and decreased, respectively, in the Hf-PS-1 group. Hf-PS-1

College of Fisheries Science, Pukyong National University, Busan, Republic of Korea 1 Corresponding author: Taek-Jeong Nam, E-mail address: [email protected]

Advances in Food and Nutrition Research, Volume 64 ISSN 1043-4526, DOI: 10.1016/B978-0-12-387669-0.00011-9

O 2011 Elsevier Inc. All rights reserved.

reduced ethanol-induced gastric injury. In in vitro assay, ethanol induced IEC-6 cells' death in a dose-dependent manner. Ethanol decreased the phosphorylation of Shc and the binding of Grb2 to Shc, and Hf-PS-1 pretreatment increased them. Ethanol also induced the phosphorylation of JNK and extracellular signal-regulated kinase (ERK), whereas Hf-PS-1 pretreatment decreased JNK activation but not ERK. Co-treatment with JNK inhibitor and ethanol decreased GSH levels, indicating that JNK phosphorylation is a critical factor during ethanol-induced injury. Therefore, Hf-PS-1 may be useful to protect against ethanol-induced gastrointestinal injury.

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