Since a high intake of fruits and vegetables is inversely related to the incidence of several degenerative diseases, the importance of a balanced diet in relation to human health has received increased consumer attention worldwide. Strawberries (Fragaria X ananassa, Duch.) are a rich source of a wide variety of nutritive compounds such as sugars, vitamins, and minerals, as well as non-nutritive, bioactive compounds such as flavonoids, anthocyanins and phenolic acids. All of these compounds exert a synergistic and cumulative effect on human health promotion and in disease prevention. Strawberry phenolics are indeed able (i) to detoxify free radicals blocking their production, (ii) to modulate the expression of genes involved in metabolism, cell survival and proliferation and antioxidant defense, and (iii) to protect and repair DNA damage. The overall objective of the present review is to update and discuss the key findings, from recent in vivo studies, on the effects of strawberries on human health. Particular attention will be paid to the molecular mechanisms proposed to explain the health effects of polyphenols against the most common diseases related to oxidative stress driven pathologies, such as cancer, cardiovascular diseases, type II diabetes, obesity and neurodegenerative diseases, and inflammation.

The potential health benefits associated with dietary intake of fruits have attracted increasing interest. Among berries, the strawberry is a rich source of several nutritive and non-nutritive bioactive compounds, which are implicated in various health-promoting and disease preventive effects. A plethora of studies have examined the benefits of strawberry consumption, such as prevention of inflammation disorders and oxidative stress, reduction of obesity related disorders and heart disease risk, and protection against various types of cancer. This review provides an overview of their nutritional and non-nutritional bioactive compounds and which factors affect their content in strawberries. In addition, the bioavailability and metabolism of major strawberry phytochemicals as well as their actions in combating many pathologies, including cancer, metabolic syndrome, cardiovascular disease, obesity, diabetes, neurodegeneration, along with microbial pathogenesis have been reviewed, with a particular attention to human studies.

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Abstract:Colon cancer is one of the most prevalent diseases across the world. Numerous epidemiological studies indicate that diets rich in fruit, such as berries, provide significant health benefits against several types of cancer, including colon cancer. The anticancer activities of berries are attributed to their high content of phytochemicals and to their relevant antioxidant properties. In vitro and in vivo studies have demonstrated that berries and their bioactive components exert therapeutic and preventive effects against colon cancer by the suppression of inflammation, oxidative stress, proliferation and angiogenesis, through the modulation of multiple signaling pathways such as NF-κB, Wnt/β-catenin, PI3K/AKT/PKB/mTOR, and ERK/MAPK. Based on the exciting outcomes of preclinical studies, a few berries have advanced to the clinical phase. A limited number of human studies have shown that consumption of berries can prevent colorectal cancer, especially in patients at high risk (familial adenopolyposis or aberrant crypt foci, and inflammatory bowel diseases). In this review, we aim to highlight the findings of berries and their bioactive compounds in colon cancer from in vitro and in vivo studies, both on animals and humans. Thus, this review could be a useful step towards the next phase of berry research in colon cancer.

Current evidence indicates that the consumption of strawberries, a natural source of a wide range of nutritive and bioactive compounds, is associated with the prevention and improvement of chronic-degenerative diseases. Studies involving cells and animals provide evidence on the anti-inflammatory, anticarcinogenic and antiproliferative activity of the strawberry. Epidemiological and clinical studies demonstrate that its acute consumption increases plasma antioxidant capacity, improves circulating inflammatory markers and ameliorates postprandial glycemic response. At the same time, a protracted intake reduces chronic inflammation and improves plasma lipid profile, supporting cardiovascular health, especially in individuals with increased risk for metabolic syndrome. To explain these beneficial effects, much attention has been paid in the past to the antioxidant properties of strawberry polyphenols. However, recent research has shown that their biological and functional activities are related not only to the antioxidant capacity but also to the modulation of many cellular pathways involved in metabolism, survival, proliferation, and antioxidant defenses. The aim of this review is to update and discuss the molecular and cellular mechanisms proposed in recent studies to elucidate the healthy effects of strawberry polyphenols against the most common chronic diseases, such as cancer, cardiovascular diseases, metabolic syndrome, and inflammation.

Numerous investigations have been made on plant phenolic compounds and cancer prevention in recent decades. Manuka honey (MH) represents a good source of phenolic compounds such as luteolin, kaempferol, quercetin, gallic acid and syringic acid. The aim of this work was to evaluate the chemopreventive effects of MH on human colon cancer HCT-116 and LoVo cells. Both cells were exposed to different concentrations of MH (0-20 mg mL-1 for HCT-116 cells and 0-50 mg mL-1 for LoVo cells) for 48 h to measure apoptosis and cell cycle arrest as well as apoptosis and cell cycle regulatory gene and protein expression. MH exhibited profound inhibitory effects on cellular growth by reducing the proliferation ability, inducing apoptosis and arresting the cell cycle in a dose-dependent manner. Interestingly, MH treatment in non-malignant cells did not exert any significant toxicity at similar concentrations. The apoptosis event was associated with the increasing expression of p53, cleaved-PARP and caspase-3 and with the activation of both intrinsic (caspase-9) and extrinsic (caspase-8) apoptotic pathways. MH induced cell cycle arrest in the S phase in HCT-116 cells, and simultaneously, in LoVo cells, it occurred in the G2/M phase through the modulation of cell cycle regulator genes (cyclin D1, cyclin E, CDK2, CDK4, p21, p27 and Rb). The expression of p-Akt was suppressed while the expression of p-p38MAPK, p-Erk1/2 and endoplasmic stress markers (ATF6 and XBP1) was increased for apoptosis induction. Overall, these findings indicate that MH could be a promising preventive or curative food therapy for colon cancer.

This study investigates the protective effect of the Sveva strawberry polyphenol-rich extract on human dermal fibroblasts against AAPH-induced oxidative stress. The HPLC-DAD/ESI-MS analysis was used for evaluating the phenolic composition of the fruits. Sveva strawberry presented a high anthocyanin content (639.79 mg per kg fresh fruit), representing ∼86.08% of the total phenolic content, with Pg-3-glc as the most abundant representative (611.18 mg per kg fresh fruit). Only one ellagitannin (agrimoniin) was identified, while two quercetins, three kaempherol derivates, and three ellagic acid derivatives were detected and quantified. Strawberry pre-treatment (0.5 mg ml(-1)) markedly increased human dermal fibroblast viability, with a significant reduction of apoptotic and dead cells, and suppressed AAPH-induced ROS generation, after only 30 minutes of incubation with the oxidizing agent, and lipid peroxidation, against a range of AAPH concentrations tested. Notably, the strawberry extract also improved the mitochondrial functionality: the basal respiratory performance after treatment was ∼1.59-fold higher compared to control cells, while pre-treatment with strawberry extract before oxidative damage increased ∼2.70-fold compared to stressed cells. Our results confirm that the strawberry possesses antioxidant properties, and may be useful for the prevention of free radical-induced skin damage.