6-Gingerol delays tumorigenesis in benzo[a]pyrene and dextran sulphate sodium-induced colorectal cancer in mice

• Published in: Food and chemical toxicology Vol. 142; p. 111483
• Main Authors: Farombi, Ebenezer O., Ajayi, Babajide O., Adedara, Isaac A.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2020
• Subjects: 6-Gingerol; Angiogenesis; Animals; Benzo(a)pyrene - toxicity; beta Catenin - metabolism; Catechols - pharmacology; Cell cycle; Colorectal cancer; Colorectal Neoplasms - chemically induced; Colorectal Neoplasms - pathology; Colorectal Neoplasms - prevention & control; Dextran Sulfate - toxicity; Disease Progression; Fatty Alcohols - pharmacology; Genes, APC; Inflammation; Male; Mice; Mice, Inbred BALB C; Neovascularization, Pathologic - prevention & control; Vascular Endothelial Growth Factor A - metabolism; Wnt/βCatenin signaling; Angiogenesis; Inflammation; 6-Gingerol; Wnt/βCatenin signaling; Colorectal cancer; Cell cycle
• DOI: 10.1016/j.fct.2020.111483
• ISSN: 0278-6915

Colorectal cancer (CRC) has been linked to dietary consumption of benzo[a]pyrene (B[a]P). 6-Gingerol (6-G), a component of ginger has been reported to possess anti-inflammatory and antioxidant activities, but little is known regarding the mechanism of 6-G in CRC chemoprevention. We therefore investigated the effect of 6-G on B[a]P. and dextran sulphate sodium (DSS) induced CRC in mice. Mice in Group I and Group II received corn oil and 6-G orally at 2 ml/kg and 100 mg/kg, respectively for 126 days. Group III were administered 125 mg/kg of B[a]P for 5 days followed by 3 cycles of 4% dextran sulphate sodium (DSS). Group IV received 6-G for 7 days followed by co-administration with 125 mg/kg of B[a]P. for 5 days and 3 cycles of 4% DSS. Tumor formation was reduced and expression of Ki-67, WNT3a, DVL-2 and β-catenin following 6-G exposure. Also, 6-G increases expression of APC, P53, TUNEL positive nuclei and subsequently decreased the expression of TNF-α, IL-1β, INOS, COX-2 and cyclin D1. 6-G inhibited angiogenesis by decreasing the concentration of VEGF, Angiopoietin-1, FGF and GDF-15 in the colon of B[a]P. and DSS exposed mice. Overall, 6-G attenuated B[a]P and DSS-induced CRC in mice via anti-inflammatory, anti-proliferative and apoptotic mechanisms. •6-Gingerol's (6-G) role on BaP and dextran sulphate sodium (DSS)-induced CRC in mice was investigated.•6-G exposure, RED tumor formation and expression of β-catenin in the colon of BaP and DSS exposed mice.•6-G increases expression of APC, and decreased the expression of of inflammatory markers.•6-G inhibited angiogenesis by decreasing the concentration of VEGF.•Thus, 6-G attenuated CRC in mice via anti-inflammatory, anti-proliferative and apoptotic mechanisms.