Blackberry
Blackberry, black raspberry, blueberry, cranberry, red raspberry, and strawberry extracts inhibit growth and stimulate apoptosis of human cancer cells in vitro
1: J Agric Food Chem. 2006 Dec 13;54(25):9329-39.
Blackberry, black raspberry, blueberry, cranberry, red raspberry, and strawberry extracts inhibit growth and stimulate apoptosis of human cancer cells in vitro.
Center for Human Nutrition, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. nseeram@mednet.ucla.edu
Berry fruits are widely consumed in our diet and have attracted much attention due to their potential human health benefits. Berries contain a diverse range of phytochemicals with biological properties such as antioxidant, anticancer, anti-neurodegerative, and anti-inflammatory activities. In the current study, extracts of six popularly consumed berries--blackberry, black raspberry, blueberry, cranberry, red raspberry and strawberry--were evaluated for their phenolic constituents using high performance liquid chromatography with ultraviolet (HPLC-UV) and electrospray ionization mass spectrometry (LC-ESI-MS) detection. The major classes of berry phenolics were anthocyanins, flavonols, flavanols, ellagitannins, gallotannins, proanthocyanidins, and phenolic acids. The berry extracts were evaluated for their ability to inhibit the growth of human oral (KB, CAL-27), breast (MCF-7), colon (HT-29, HCT116), and prostate (LNCaP) tumor cell lines at concentrations ranging from 25 to 200 micro g/mL. With increasing concentration of berry extract, increasing inhibition of cell proliferation in all of the cell lines were observed, with different degrees of potency between cell lines. The berry extracts were also evaluated for their ability to stimulate apoptosis of the COX-2 expressing colon cancer cell line, HT-29. Black raspberry and strawberry extracts showed the most significant pro-apoptotic effects against this cell line. The data provided by the current study and from other laboratories warrants further investigation into the chemopreventive and chemotherapeutic effects of berries using in vivo models.
Cyanidin-3-glucoside, a natural product derived from blackberry, exhibits chemopreventive and chemotherapeutic activity
1: J Biol Chem. 2006 Jun 23;281(25):17359-68. Epub 2006 Apr 17.
Cyanidin-3-glucoside, a natural product derived from blackberry, exhibits chemopreventive and chemotherapeutic activity.
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA. mid5@cdc.gov
Epidemiological data suggest that consumption of fruits and vegetables has been associated with a lower incidence of cancer. Cyanidin-3-glucoside (C3G), a compound found in blackberry and other food products, was shown to possess chemopreventive and chemotherapeutic activity in the present study. In cultured JB6 cells, C3G was able to scavenge ultraviolet B-induced *OH and O2-* radicals. In vivo studies indicated that C3G treatment decreased the number of non-malignant and malignant skin tumors per mouse induced by 12-O-tetradecanolyphorbol-13-acetate (TPA) in 7,12-dimethylbenz[a]anthracene-initiated mouse skin. Pretreatment of JB6 cells with C3G inhibited UVB- and TPA-induced transactivation of NF-kappaB and AP-1 and expression of cyclooxygenase-2 and tumor necrosis factor-alpha. These inhibitory effects appear to be mediated through the inhibition of MAPK activity. C3G also blocked TPA-induced neoplastic transformation in JB6 cells. In addition, C3G inhibited proliferation of a human lung carcinoma cell line, A549. Animal studies showed that C3G reduced the size of A549 tumor xenograft growth and significantly inhibited metastasis in nude mice. Mechanistic studies indicated that C3G inhibited migration and invasion of A549 tumor cells. These finding demonstrate for the first time that a purified compound of anthocyanin inhibits tumor promoter-induced carcinogenesis and tumor metastasis in vivo.
PMID: 16618699 [PubMed - indexed for MEDLINE]
Inhibition of nitric oxide biosynthesis by anthocyanin fraction of blackberry extract.
1: Nitric Oxide. 2006 Aug;15(1):30-9. Epub 2006 Mar 6.
Inhibition of nitric oxide biosynthesis by anthocyanin fraction of blackberry extract.
Department of Experimental Pharmacology, University of Naples Federico II, Italy.
Anthocyanins are natural colorant belonging to the flavonoid family, widely distributed among flowers, fruits, and vegetables. Some flavonoids have been found to possess anticarcinogenic, cytotoxic, cytostatic, antioxidant, and anti-inflammatory properties. Since increased nitric oxide (NO) plays a role in inflammation, we have investigated whether the pharmacological activity of the anthocyanin fraction of a blackberry extract (cyanidin-3-O-glucoside representing about 88% of the total anthocyanin content) was due to the suppression of NO synthesis. The markedly increased production of nitrites by stimulation of J774 cells with lipopolysaccharide (LPS) for 24 h was concentration-dependently inhibited by the anthocyanin fraction (11, 22, 45, and 90 microg/ml) of the extract. Moreover, this inhibition was dependent on a dual mechanism, since the extract attenuated iNOS protein expression and decreased the iNOS activity in lungs from LPS-stimulated rats. Inhibition of iNOS protein expression appeared to be at the transcriptional level, since the extract and similarly cyanidin-3-O-glucoside (10, 20, 40, and 80 microg/ml, amounts corresponding to the concentrations present in the extract) decreased LPS-induced NF-kappaB activation, through inhibition of IkappaBalpha degradation, and reduced ERK-1/2 phosphorylation in a concentration-dependent manner. In conclusion, our study demonstrates that at least some part of the anti-inflammatory activity of blackberry extract is due to the suppression of NO production by cyanidin-3-O-glucoside, which is the main anthocyanin present in the extract. The mechanism of this inhibition seems to be due to an action on the expression/activity of the enzyme. In particular, the protein expression was inhibited through the attenuation of NF-kappaB and/or MAPK activation.
PMID: 16517190 [PubMed - indexed for MEDLINE]
Blackberry extracts inhibit activating protein 1 activation and cell transformation by perturbing the mitogenic signaling pathway
1: Nutr Cancer. 2004;50(1):80-9.
Blackberry extracts inhibit activating protein 1 activation and cell transformation by perturbing the mitogenic signaling pathway.
Pathology and Physiology Research Branch, Helath Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Blackberries are natural rich sources of bioflavonoids and phenolic compounds that are commonly known as potential chemopreventive agents. Here, we investigated the effects of fresh blackberry extracts on proliferation of cancer cells and neoplastic transformation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), as well as the underlying mechanisms of signal transduction pathways. Using electron spin resonance, we found that blackberry extract is an effective scavenger of free radicals, including hydroxyl and superoxide radicals. Blackberry extract inhibited the proliferation of a human lung cancer cell line, A549. Pretreatment of A549 cells with blackberry extract resulted in an inhibition of 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation induced by ultraviolet B (UVB) irradiation. Blackberry extract decreased TPA-induced neoplastic transformation of JB6 P+ cells. Pretreatment of JB6 cells with blackberry extract resulted in the inhibition of both UVB- and TPA-induced AP-1 transactivation. Furthermore, blackberry extract also blocked UVB- or TPA-induced phosphorylation of ERKs and JNKs, but not p38 kinase. Overall, these results indicated that an extract from fresh blackberry may inhibit tumor promoter-induced carcinogenesis and associated cell signaling, and suggest that the chemopreventive effects of fresh blackberry may be through its antioxidant properties by blocking reactive oxygen species-mediated AP-1 and mitogen-activated protein kinase activation.
PMID: 15572301 [PubMed - indexed for MEDLINE]
Anthocyanins are efficiently absorbed from the small intestine in rats
1: J Nutr. 2004 Sep;134(9):2275-9.
Anthocyanins are efficiently absorbed from the small intestine in rats.
Laboratoire de Pharmacognosie, Faculte de Pharmacie, 63001 Clermont-Ferrand, France. Severine.Talafera@u-clermont1.fr
Anthocyanins are natural pigments that possess antioxidant activities and are implicated in various health effects. Recent studies showed that the stomach is a site of anthocyanin absorption. However, the fate of anthocyanins in the small intestine remains unknown. We therefore investigated anthocyanin absorption after in situ perfusion of the jejunum + ileum in rats. The intestine was perfused for 45 min with a physiological buffer supplemented with various anthocyanins. Purified anthocyanin glycosides (9.2 nmol/min) or blackberry (9.0 nmol/min) or bilberry (45.2 nmol/min) anthocyanins were perfused. A high proportion of anthocyanin glycosides was absorbed through the small intestine after perfusion. The rate of absorption was influenced by the chemical structure of the anthocyanin and varied from 10.7 (malvidin 3-glucoside) to 22.4% (cyanidin 3-glucoside). Regardless of the anthocyanins perfused, only glycosides were recovered in the intestinal lumen. After perfusion of a high amount of blackberry anthocyanins (600 nmol/min), native cyanidin 3-glucoside was recovered in urine and plasma from the aorta and mesenteric vein. Methylated and/or glucuronidated derivatives were also identified. Analysis of bile samples revealed that cyanidin 3-glucoside and its methylated derivatives (peonidin 3-glucoside + peonidin glucuronide) quickly appeared in bile. This study demonstrated that anthocyanin glycosides are rapidly and efficiently absorbed from the small intestine. Furthermore, anthocyanins are quickly metabolized and excreted into bile and urine as intact glycosides as well as methylated forms and glucuronidated derivatives.
PMID: 15333716 [PubMed - indexed for MEDLINE]
