Effect of ginger root on cyclooxygenase-1 and 15-hydroxyprostaglandin dehydrogenase expression in colonic mucosa of humans at normal and increased risk for colorectal cancer

• Published in: European journal of cancer prevention Vol. 22; no. 5; p. 455
• Main Authors: Jiang, Yan, Turgeon, Danielle K, Wright, Benjamin D, Sidahmed, Elkhansa, Ruffin, Mack T, Brenner, Dean E, Sen, Ananda, Zick, Suzanna M
• Format: Journal Article
• Language: English
• Published: England 01.09.2013
• Subjects: Adult; Carcinoma in Situ - genetics; Carcinoma in Situ - metabolism; Carcinoma in Situ - pathology; Colon - drug effects; Colon - metabolism; Colon - pathology; Colorectal Neoplasms - genetics; Colorectal Neoplasms - metabolism; Colorectal Neoplasms - pathology; Cyclooxygenase 1 - genetics; Female; Gene Expression Regulation, Enzymologic - drug effects; Health; Humans; Hydroxyprostaglandin Dehydrogenases - genetics; Intestinal Mucosa - drug effects; Intestinal Mucosa - metabolism; Male; Middle Aged; Placebos; Plant Extracts - pharmacology; Plant Roots - chemistry; Precancerous Conditions - genetics; Precancerous Conditions - metabolism; Precancerous Conditions - pathology; Risk Factors; Young Adult; Zingiber officinale - chemistry
• ISSN: 1473-5709
• DOI: 10.1097/cej.0b013e32835c829b

Elevated tissue levels of prostaglandin E2, produced by cyclooxygenase (COX), are an early event in colorectal cancer (CRC). Data suggest the efficacy of nonsteroidal anti-inflammatory drugs, such as cancer preventives, in the inhibition of COX activity; however, side effects of nonsteroidal anti-inflammatory pose unacceptable limitations. Ginger has been reported to have anti-inflammatory activities with significant CRC preventive potential. We investigated whether consumption of 2.0 g ginger daily regulated the level of two key enzymes that control prostaglandin E2 production, COX-1 and NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Thirty participants at normal and 20 participants at increased risk for CRC were randomized and given 2.0 g/day ginger or placebo for 28 days. Flexible sigmoidoscopy was used to obtain colon biopsies at baseline and the end of the study. Tissue levels of COX-1 and 15-PGDH were assessed using western blotting. After ginger consumption, participants at increased risk for CRC had a significantly reduced colonic COX-1 protein level (23.8±41%) compared with the placebo group (18.9±52%; P=0.03). Protein levels of 15-PGDH in the colon were unchanged. In participants who were at normal risk for CRC, neither protein levels of COX-1 nor 15-PGDH in the colon were altered by ginger consumption. Ginger significantly lowered COX-1 protein expression in participants at increased risk for CRC but not in those at normal risk for CRC. Ginger did not alter 15-PGDH protein expression in either increased or normal-risk participants. Further investigation, in larger studies with a longer ginger intervention, is needed to examine the ability of ginger to impact tissue levels of prostaglandin.