Molecular Mechanisms Behind the Chemopreventive Effects of Anthocyanidins

Abstract

Anthocyanins are polyphenolic ring-based flavonoids, and are widespread in fruits and vegetables of red-blue color. Epidemiological investigations and animal experiments have indicated that anthocyanins may contribute to cancer chemoprevention. The studies on the mechanism have been done recently at molecular level. This review summarizes current molecular bases for anthocyanidins on several key steps involved in cancer chemoprevention: (i) inhibition of anthocyanidins in cell transformation through targeting mitogen-activated protein kinase (MAPK) pathway and activator protein 1 (AP-1) factor; (ii) suppression of anthocyanidins in inflammation and carcinogenesis through targeting nuclear factor kappa B (NF- $\kappa$ B) pathway and cyclooxygenase 2 (COX-2) gene; (iii) apoptotic induction of cancer cells by anthocyanidins through reactive oxygen species (ROS) / c-Jun NH(2)-terminal kinase (JNK)-mediated caspase activation. These data provide a first molecular view of anthocyanidins contributing to cancer chemoprevention.

Figure 1

Basic chemical structures of the major anthocyanidins.

Figure 2

A schematic molecular view of cancer chemoprevention by anthocyanidins. Anthocyanidins may contribute to cancer chemoprevention through targeting three different signal transduction pathways and downstream genes. Abbreviations: AP-1, activator protein-1; ERK, extracellular signal-regulated kinase; JNK, c-Jun NH₂-terminal kinase; LPS, lipopolysaccharide; NF-κB, nuclear factor κB; ROS, reactive oxygen species; TPA, 12-O-tetradecanoylphorbol-13-acetate.