Long-Term Oral Administration of Piceatannol (3,5,3',4'-Tetrahydroxystilbene) Attenuates Colon Tumor Growth Induced by Azoxymethane Plus Dextran Sulfate Sodium in C57BL/6J Mice.

Abstract

AIM:

The effects of 3,5,3',4'-tetrahydroxystilbene (piceatannol) on azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colon cancer growth and changes in IL-1β, IL-6, tumor necrosis factor-α (cytokines), MCP-1, vascular endothelial growth factor, and PD-1 colon levels were investigated herein.

METHODS:

AOM (10 mg/kg, i.p.) on day 0 induced colorectal carcinogenesis. On day 3, mice were provided with water containing 1.5% (w/v) DSS ad libitum for 3 day, and this 3-day drinking protocol was repeated twice. Piceatannol (5 and 12.5 mg/kg, twice daily) was orally administered to mice for 7-, 7-, 7-, and 6-day and then discontinued for 14-, 15-, and 16-day. Cytokines, chemokine, and PD-1 colon levels were measured by the respective ELISA kits.

RESULTS:

In mice administered piceatannol (12.5 mg/kg), the tumor number, tumor area, and Ki-67-positive cell numbers decreased by 30.1%, 57.2%, and 89.1%, respectively, colon MCP-1 and PD-1 levels showed reductions of 43.8% and 70.9%, respectively, and COX-2-positive cell numbers declined by 60.2%.

CONCLUSIONS:

The inhibitory effects of piceatannol on AOM/DSS-induced colon tumor growth appear to be associated with reductions in colon MCP-1 and PD-1 levels through the downregulated expression of COX-2 in the tumor microenvironment.

• Authors: Yoshiyuki Kimura
• Journal: Nutrition and cancer (Nutr Cancer) Vol. 74 Issue 6 Pg. 2184-2195 ( 2022) ISSN: 1532-7914 [Electronic] United States
• PMID: 34622729 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cytokines
• Programmed Cell Death 1 Receptor
• Stilbenes
• Vascular Endothelial Growth Factor A
• 3,3',4,5'-tetrahydroxystilbene
• Dextran Sulfate
• Cyclooxygenase 2
• Azoxymethane

Topics

• Administration, Oral
• Animals
• Azoxymethane (toxicity)
• Colitis (chemically induced)
• Colon (metabolism)
• Colonic Neoplasms (chemically induced, drug therapy, metabolism)
• Cyclooxygenase 2 (metabolism)
• Cytokines (metabolism)
• Dextran Sulfate (toxicity)
• Disease Models, Animal
• Mice
• Mice, Inbred C57BL
• Programmed Cell Death 1 Receptor (metabolism)
• Stilbenes
• Tumor Microenvironment
• Vascular Endothelial Growth Factor A (metabolism)