Polyphenolic flavonoids are considered natural, non-toxic chemopreventers, which are most commonly derived from plants, fruits, and vegetables. Most of these polyphenolics exhibit remarkable antioxidant, anti-inflammatory, and anticancer properties. Quercetin (Qu) is a chief representative of these polyphenolic compounds, which exhibits excellent antioxidant and anticancer potential, and has attracted the attention of researchers working in the area of cancer biology. Qu can regulate numerous tumor-related activities, such as oxidative stress, angiogenesis, cell cycle, tumor necrosis factor, proliferation, apoptosis, and metastasis. The anticancer properties of Qu mainly occur through the modulation of vascular endothelial growth factor (VEGF), apoptosis, phosphatidyl inositol-3-kinase (P13K)/Akt (proteinase-kinase B)/mTOR (mammalian target of rapamycin), MAPK (mitogen activated protein kinase)/ERK1/2 (extracellular signal-regulated kinase 1/2), and Wnt/β-catenin signaling pathways. The anticancer potential of Qu is documented in numerous in vivo and in vitro studies, involving several animal models and cell lines. Remarkably, this phytochemical possesses toxic activities against cancerous cells only, with limited toxic effects on normal cells. In this review, we present extensive research investigations aimed to discuss the therapeutic potential of Qu in the management of different types of cancers. The anticancer potential of Qu is specifically discussed by focusing its ability to target specific molecular signaling, such as p53, epidermal growth factor receptor (EGFR), VEGF, signal transducer and activator of transcription (STAT), PI3K/Akt, and nuclear factor kappa B (NF-κB) pathways. The anticancer potential of Qu has gained remarkable interest, but the exact mechanism of its action remains unclear. However, this natural compound has great pharmacological potential; it is now believed to be a complementary—or alternative—medicine for the prevention and treatment of different cancers.

Tamarix aphylla is a commonly grown plant in Saudi Arabia and its therapeutic potential is widely recognized. Here, in this study, the aim was to explore the role of T. aphylla leaf extract (TAE) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and LPS-stimulated RAW 264.7 cells. The antioxidant and anti-inflammatory parameters of TAE were performed through in vitro assays by measuring H₂O₂ free radical scavenging and protein denaturation inhibition. After LPS administration, broncho alveolar lavage fluid (BALF) and lung tissue were obtained to evaluate the pro-inflammatory cytokine levels, histopathological alterations, immunohistochemistry and TUNEL staining. The results designate that TAE shows anti-inflammatory activity through a decrease in pro-inflammatory cytokines, TNF-α and IL-6 in LPS-stimulated RAW 264.7 cells and BALF. The antioxidant enzyme level (SOD) decreased and MDA content was increased in the LPS-induced mice. However, TAE pretreatment markedly reversed these parameters compared to the group administered LPS only (p < 0.05). The histopathological analysis demonstrated that TAE maintained the lung tissue architecture by reducing LPS-induced inflammation and congestion. The expression pattern of the Cox-2 protein and apoptosis was high in the group administered LPS only, whereas TAE pretreatment showed a reduction in the expression pattern and apoptosis. Moreover, the in vitro assay of TAE demonstrated a concentration-dependent free radical scavenging and anti-inflammatory activity. In conclusion, our results advocate the health-promoting effects of T. aphylla on LPS-induced acute lung injury, which might be due to its antioxidative and anti-inflammatory potential.

A polyphenolic component of ginger, 6-gingerol, is widely reported to possess antioxidant, anti-inflammatory and anticancer activities. In the current study, it was aimed to investigate the anticancer effects of 6-gingerol (6-Gin) on azoxymethane (AOM)-induced colon cancer in rats. The results reveal that 6-Gin treatment significantly improves the antioxidant status disturbed by AOM intoxication. The 6-Gin treatment animal group showed enhanced activity of catalase (CAT) (46.6 ± 6.4 vs. 23.3 ± 4.3 U/mg protein), superoxide dismutase (SOD) (81.3 ± 7.6 vs. 60.4 ± 3.5 U/mg protein) and glutathione-S-transferase (GST) (90.3 ± 9.4 vs. 53.8 ± 10 mU/mg protein) (p < 0.05) as compared to the disease control group. Furthermore, the results reveal that AOM significantly enhances the inflammatory response and 6-gingerol potentially attenuates this response, estimated by markers, such as tumor necrosis factor-α (TNF-α) (1346 ± 67 vs. 1023 ± 58 pg/g), C-reactive protein (CRP) (1.12 ± 0.08 vs. 0.92 ± 0.7 ng/mL) and interleukin-6 (IL-6) (945 ± 67 vs. 653 ± 33 pg/g). In addition, the lipid peroxidation estimated in terms of malondialdehyde (MDA) provoked by AOM exposure is significantly reduced by 6-gingerol treatment (167 ± 7.5 vs. 128.3 nmol/g). Furthermore, 6-gingerol significantly maintains the colon tissue architecture disturbed by the AOM treatment. Loss of tumor suppressor protein, phosphatase and tensin homolog (PTEN) expression was noticed in the AOM treated group, whereas in the animals treated with 6-gingerol, the positivity of PTEN expression was high. In conclusion, the current findings advocate the health-promoting effects of 6-gingerol on colon cancer, which might be due to its antioxidant and anti-inflammatory potential.

Celery (Appium graveolens L.) and parsley (Petroselinum crispum (Mill.) Fuss) are herbs utilized in the everyday diet as spices and culinary flavorings, often used in the chemical and medicinal industries. Despite the knowing benefits of different plants from the Apiaceae family, their chemical composition is closely associated with various extrinsic factors. Environmental loading with trace elements (TEs) can modify a plant’s metabolic pathways, change bioactive compounds production, cause plant pollution, and consequently provoke human health issues. Therefore, we established this research aiming to unravel the linkage between TEs accumulation and phenolic status in celery and parsley. Higher As, Cd, and Ni levels were observed in celery, which was followed by greater DPPH^∙ radical scavenging activity and higher coumarins content. Contrary, parsley accumulated chromium to a greater extent, was richer in flavonoids, apigenin, and its glucosides. No significant difference between species was found in total phenolic contents, where ferulic and chlorogenic acid dominated in both species. A direct relationship between TEs and selected secondary metabolites was proven by the standardized major axis model. Besides abundant bioactive compounds, analyzed plant species showed a moderate hazard index in the children population, since the hazard index was higher than 1. Therefore, future perspectives should be turned towards the production of genotypes with a lower potential for toxic elements accumulation, so the health benefits of plant food will be more prominent.

Chronic respiratory diseases are a leading cause of lung-related death worldwide. The vital factors causing lung pathogenesis include consistent exposure to tobacco smoke, air pollution, and occupational risks. Regarding the significant morbidity and mortality linked to lung pathogenesis, there are neither conclusive treatments nor wholly preventive strategies. In the present study, the protective mechanism of Ajwa date extract (ADE), on Benzopyrene [B(a)P]-induced lung injury in animal models was investigated using antioxidant, lipid peroxidation, anti-inflammatory activities, angiogenesis, histopathological studies, and apoptosis assays. B(a)P treatment significantly decreased the level of antioxidant enzymes such as catalase (Cat) (13.4 vs. 24.7 U/mg protein), Superoxide dismutase (SOD) (38.5 vs. 65.7 U/mg protein), Glutathione peroxidase (GPx) (42.4 vs. 57.3 U/mg protein) and total antioxidant capacity (TAC) (49.8 vs. 98.7 nM) as compared to the treatment group (p < 0.05). B(a)P treatment led to increased expression of pro-inflammatory markers such as TNF-α (88.5 vs. 72.6 pg/mL), IFN-γ (4.86 vs. 3.56 pg/mL), interleukin-6 (IL-6) (109.6 vs. 85.4 pg/mL) and CRP (1.84 vs. 0.94 ng/mL) as compared to the treatment group (p < 0.05). The data shows a significant increase in lipid peroxidation and angiogenesis factors such as vascular endothelial growth factor (VEGF) by B(a)P treatment (p < 0.05). However, ADE treatment showed an improvement of these factors. In addition, ADE treatment significantly ameliorated histopathological changes, collagen fiber deposition, and expression pattern of VEGF and Bax proteins. Furthermore, the flow cytometry data demonstrated that B(a)P intoxication enhanced the apoptosis ratio, which was significantly improved with ADE treatment. Finally, we may infer that Phyto-constituents of ADE have the potential to protect against B(a)P-induced lung pathogenesis. Therefore, Ajwa dates might be used to develop a possible potent alternative therapy for lung pathogenesis.

Breast cancer can be categorized as a commonly occurring cancer among women with a high mortality rate. Due to the repetitive treatment cycles, it has been noted that the patients develop resistance towards the chemotherapeutic drugs and remain unresponsive towards them. Therefore, many researchers are studying various signaling pathways involved in drug resistance for cancer treatment to overcome the obstacle. Hippo signaling is a widely studied pathway involved in tumor progression and controlling cell proliferation. Hence, understanding the aspects of the gene involved Hippo pathway would provide an insight into the mechanism behind the resistance and result in the development of new treatments. Here, we review the Hippo signaling pathway in humans and how the expression of different components leads to the regulation of resistance against some of the common chemo-drugs used in breast cancer treatment. The article will also discuss the chemotherapeutics that became ineffective due to the resistance and the mechanism following the process.