Anthocyanins have anticancer action, according to rapidly increasing laboratory and clinical studies, and bilberry anthocyanins are being studied as chemopreventive drugs.
Anthocyanins have been shown to upregulate tumour suppressor genes, cause apoptosis in cancer cells, repair and protect genomic DNA integrity, which is crucial in decreasing age-related oxidative stress, and enhance neuronal and cognitive brain function, among other things.
Despite their limited bioavailability, bilberry anthocyanins offer significant health benefits.
In 25 colorectal cancer patients, bilberry anthocyanins were found to be potent cancer preventative agents. (Thomasset,2009). Upregulation of tumour suppressor genes and intracellular signalling cascades are frequent biological targets for anthocyanins in cancer cells treated with anthocyanins.
A defect in apoptosis has been identified as a key cause of treatment resistance. In B-cell chronic lymphocytic leukaemia (B-CLL), anthocyanins triggered apoptosis in cancer cells via activating redox-sensitive caspase 3-pathways, but had no impact in normal peripheral blood cells.
Bilberry extracts also demonstrated significant pro-apoptotic activity in B-CLL cells via a redox-sensitive caspase 3 activation-related mechanism requiring deregulation of the Bad/Bcl-2 pathway. Bilberry anthocyanins also inhibit the proliferation and invasive capability of human non-small-cell lung cancer cells in a synergistic manner.
The creation of a more effective delivery method for Bilberry anthocyanins would improve their cancer preventive and therapy effectiveness substantially.
Phenolic chemicals, which are abundant in Bilberries (Vaccinium myrtillus) and a range of other plants such as lingonberries (Vacciniumvitis-idaea) and cloudberries (Rubus chamaemorus), are the most promising anticarcinogenic agents in plants. Anthocyanins are hydrophilic chemicals that cannot penetrate the plasma membrane of a cell through passive diffusion.
Without a hydrophilic carrier, such as the NNS, which also has a hydrophobic fatty acid component that “melts” into cell membranes to deposit the Bilberry into cancer cells, the anthocyanins’ bioavailability would be limited.
When compared to the free component, the bilberry extract had a stronger anti-cancer impact when encapsulated, according to the findings. Experiments were carried out first to see if there was an effect, and then to see when that effect was strongest. The inhibition at 72 hours was significantly stronger than at 48 hours. However, due to metabolic degradation of the anthocyanins and nutritional depletion in the cell culture, the results after 96 hours were identical to the 24 hour % inhibition curve.
Many biological effects have been documented for bilberry (European blueberry), including anticancer efficacy. We studied the antiproliferative properties of bilberry extract in MCF7 human breast cancer cells, as well as its potential to induce apoptosis and alter microtubule assembly and structure. Bilberry extract reduced cell growth in a dose-dependent manner, with a 50% inhibitory dosage of 0.3–0.4 mg/mL, in addition to inducing apoptotic cell death.
There was no specific suppression of mitosis or any other cell cycle stage at these doses, nor was there any effect on the microtubule or actin cytoskeleton. Higher extract concentrations (0.5–0.9 mg/mL) did, however, result in an increase in the proportion of cells in the G2/M phase of the cell cycle, as well as microtubule breakdown and the development of punctate tubulin aggregates in the cells.
In vitro, bilberry extract at 0.3–0.4 mg/mL did not significantly inhibit microtubule polymerization, but at higher extract doses (0.5–1 mg/mL), substantial inhibition (30%) did occur. We conclude that at its lowest effective doses, bilberry extract, not simply the pure anthocyanins it contains, suppresses proliferation and causes death in breast cancer cells via a mechanism that does not require microtubules or mitosis.
In vitro, bilberry extract at 0.3–0.4 mg/mL did not significantly inhibit microtubule polymerization, but at higher extract doses (0.5–1 mg/mL), substantial inhibition (30%) did occur.
We conclude that at its lowest effective doses, bilberry extract, not simply the pure anthocyanins it contains, suppresses proliferation and causes death in breast cancer cells via a mechanism that does not require microtubules or mitosis. We also discovered that the extract, at slightly higher concentrations, alters microtubule structure in cells and promotes cell accumulation during mitosis by a direct effect on microtubules.
