The Therapeutic Potential of Anthocyanins: Current Approaches Based on Their Molecular Mechanism of Action

Abstract

Anthocyanins are natural phenolic pigments with biological activity. They are well-known to have potent antioxidant and antiinflammatory activity, which explains the various biological effects reported for these substances suggesting their antidiabetic and anticancer activities, and their role in cardiovascular and neuroprotective prevention. This review aims to comprehensively analyze different studies performed on this class of compounds, their bioavailability and their therapeutic potential. An in-depth look in preclinical, in vitro and in vivo, and clinical studies indicates the preventive effects of anthocyanins on cardioprotection, neuroprotection, antiobesity as well as their antidiabetes and anticancer effects.

Keywords: anthocyanins; anticancer; antidiabetic; antiobesity; antioxidant; biodisponibility; cardioprotective; neuroprotective.

Figure 1

Chemical structures of main anthocyanins: pelargonidin, cyanidin, peonidin, delphinidin, malvidin, and petunidin.

Figure 2

Summarized scheme of the most important pharmacological properties and molecular mechanisms of action of anthocyanins.

Figure 3

In cerebral ischemia, anthocyanins (ACNs) reduce neuroinflammation by: (i) decreasing the expression of Toll-like receptor 4 (TLR4), an activator of nuclear factor kappa B (NF-κB), and tumor necrosis factor-α (TNF-α) proinflammatory cytokine expression (Cui et al., 2018). (ii) Reducing the expression of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS), targets of NF-κB, and as a consequence NO content at cerebral level, thus reflecting a reduction in brain damage (Di Giacomo et al., 2012; Cui et al., 2018). A significant increase of eNOS was observed which may result in vasorelaxation with a consequent attenuation of the ischemic insult and promotion of functional recovery of the ischemic zone (Di Giacomo et al., 2012). (ii) Direct antiapoptotic role, since they partially blocked AIF, but not cytochrome c release from mitochondria, thus indicating that guanine nucleotide exchange factor (C3G) reduced apoptosis by suppressing a caspase-independent pathway (Min et al., 2011).