Blackcurrant (Ribes nigrum), also known as cassis, belongs to the Grossulariaceae family. Grown for its berries, this dense, bushy shrub reaches a height of 1 m to 1.5 m.
It is native to central Europe and northern Asia, with Europe accounting for 80% of global blackcurrant production. In the Middle Ages, blackcurrant was prized for its therapeutic properties, particularly as a treatment for gout. Today, the leaves, berries and buds are used in herbal medicine.
The leaves contain flavonoids (quercetin, kaempferol, catechin, epicatechin), tannins, anthocyanins (cyanidin, delphinidin, peonidin, malvidin) and phenol acids such as caffeic acid and chlorogenic acid. The berries have high levels of vitamin C and also contain polyphenols (flavonoids, anthocyanins, ellagitannins and lignans), carotenoids (β-carotene, lutein, zeaxanthin) and polysaccharides (CAPS: cassis polysaccharides). Furthermore, blackcurrant seed oil is rich in polyunsaturated fatty acids (GOPALAN & al., 2012).
Blackcurrant neutralises free radicals and inhibits lipid peroxidation. It improves cell viability, lowers levels of malondialdehyde (MDA), which is a marker of oxidative stress, and reduces cell death induced by oxygen peroxide (GARBACKI & al., 2005 ; JIA & al., 2014). It also increases the activity of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GOPALAN & al., 2012).
Blackcurrant leaves have anti-inflammatory properties and reduce carrageenan-induced inflammatory oedema in rats (DECLUME & al., 1989 ; GARBACKI & al., 2004).
Also in rats, proanthocyanidins isolated from blackcurrant leaves inhibit leukocyte infiltration. This mechanism can be explained by inhibition of endothelial cell adhesion molecules (ICAM-1 and VCAM-1) and by modulation of TNF-α-induced VEGF transcription (GARBACKI & al., 2005).
In vitro, prodelphinidins isolated from blackcurrant leaves reduce prostaglandin secretion by inhibiting cyclo-oxygenase and increase the production of cartilage tissue constituents (type II collagen and proteoglycans). They therefore play a beneficial role in osteoarthritis (GARBACKI & al., 2002).
In mice with atopic dermatitis, blackcurrant and its polysaccharides improve clinical symptoms of atopy in a dose-dependent manner. In addition, they reduce serum immunoglobulin E levels and the infiltration of mast cells into the dermis (ASHIGA & al., 2017).
Blackcurrant anthocyanins stimulate regeneration of rhodopsin, a pigment that helps the eye adapt to light and darkness, thus improving night vision. At a dose level of 50 mg/day, they alleviate the symptoms of computer work-related visual fatigue (NAKAISHI & al., 2000).
A study of blackcurrant consumption in rats and rabbits showed that intact anthocyanins are present in the cornea, aqueous humour, ciliary body, sclera and retina. This means that anthocyanins pass through the blood-retinal barrier and blood-aqueous barrier (MATSUMOTO & al., 2006).
Anthocyanins improve blood flow to the optic nerve and retina, while increasing and normalising levels of plasma endothelin-1 in glaucoma patients (OHGURO & al., 2007).
Blackcurrant improves neuronal signal transduction as measured by striatal dopamine release. In addition, the polyphenols in blackcurrant restore the brain’s ability to generate a neuroprotective response to stress in rats (SHUKITT-HAL & al., 2005). They also alleviate neuronal cell death elicited by rotenone. Plant extracts rich in anthocyanins and proanthocyanidins exhibit greater neuroprotective activity than extracts rich in other polyphenols (STRATHEARN & al., 2014).
Cassis polysaccharides (CAPS) have an immunostimulatory effect. They have macrophage-stimulating and antitumour activity and a stimulatory effect on the release of interleukin 2 (IL-2), IL-10, interferon gamma (IFN-γ) and IL-4 from splenocytes in vitro (TAKATA & al., 2005). They stimulate dendritic cells through TLR4 signalling and activate Th1-type cytokine release (ASHIGAI & al., 2017).
Blackcurrant exhibits antiviral activity in vitro and in vivo against Influenza A virus by interfering with virus internalisation, resulting in reduced viral uptake into host cells (EHRHARDT & al., 2013 ; SEKIZAWA & al., 2013 ; HAASBACH & al., 2014).
In human cells in vitro, blackcurrant limits DNA damage induced by hydrogen peroxide and therefore has an antigenotoxic effect, since it reduces genomic instability. These effects appear to be related to polyphenols, L-ascorbic acid and other antioxidant compounds (YAMAMOTO & al., 2014).
In a model of rat liver carcinogenesis, blackcurrant dose-dependently decreases the incidence, number, size and volume of preneoplastic hepatic nodules. It inhibits abnormal cell proliferation and promotes tumour cell apoptosis (BISHAYEE & al., 2011).
Spontaneously hypertensive rats fed a diet containing blackcurrant oil have been found to have lower blood pressure (ENGLER & al., 1993).
Blackcurrant has been shown to increase nitric oxide (NO) synthesis. It induces endothelium-dependent vasorelaxation via the histamine H1-receptors on the endothelium (NAKAMURA & al., 2002).
A mixture of blackcurrant, olive and fish oils reduces levels of serum thromboxane B2, a metabolite of thromboxane A2, which is a prothrombotic factor released by activated platelets. It therefore lowers the risk of thrombus formation and cardiovascular events (PREGNOLATO & al., 1996).
For a delicious pick-me-up, think blackcurrant!
