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Cholesteryl glucoside-induced protection against gastric ulcer.

Cell structure and function (2003-09-03)
Shohko Kunimoto, Wataru Murofushi, Isao Yamatsu, Yukie Hasegawa, Narie Sasaki, Susumu Kobayashi, Tetsuyuki Kobayashi, Hiromu Murofushi, Kimiko Murakami-Murofushi
RÉSUMÉ

The cytoprotective effect of heat shock proteins (HSPs) promises new therapeutic modalities for medical treatment. We examined the anti-ulcer effect of cholesteryl glucoside (1-O-cholesteryl-beta-D-glucopyranoside, CG) on cold-restraint stress-induced gastric ulcer in rats, in terms of its correlative ability to activate heat shock factor (HSF) and to induce HSP70. Rapid induction of CG occurred in animal tissues, especially in stomach, after exposure to stress, indicating that this glycolipid might act as an anti-stress, lipid mediator involved in the very early stages of stress-induced signal transduction. Orally administered CG apparently showed anti-ulcer activity in rats via HSF activation and HSP70 induction. When compared with geranylgeranylacetone (GGA), the well known as an effective, synthetic anti-ulcer agent, CG proved to have the same level of strength on ulcer inhibition. GGA caused CG and HSP70 induction in gastric mucosa, indicating that GGA induced HSP70 via CG production. CG thus might be useful for medical treatment of stress-induced diseases, and as an anti-stress supplement for daily diet.

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Sigma-Aldrich
Cholesterol β-D-glucoside, ≥97% (TLC)