Cancer is a hard-to-treat disease with a high reoccurrence rate that affects health and lives globally. The condition has a high occurrence rate and is the second leading cause of mortality after cardiovascular disorders. Increased research and more profound knowledge of the mechanisms contributing to the disease’s onset and progression have led to drug discovery and development. Various drugs are on the market against cancer; however, the drugs face challenges of chemoresistance. The other major problem is the side effects of these drugs. Therefore, using complementary and additional medicines from natural sources is the best strategy to overcome these issues. The naturally occurring phytochemicals are a vast source of novel drugs against various ailments. The modes of action by which phytochemicals show their anti-cancer effects can be the induction of apoptosis, the onset of cell cycle arrest, kinase inhibition, and the blocking of carcinogens. This review aims to describe different phytochemicals, their classification, the role of phytochemicals as anti-cancer agents, the mode of action of phytochemicals, and their role in various types of cancer.

Tamarix aphylla is a well-known species of the genus Tamarix. T. aphylla (Tamaricaceae) is a perennial tree in Asia, the Middle East, and Central Africa. It is used as a carminative diuretic in tuberculosis, leprosy, and hepatitis. Various pharmacological properties have been shown by T. aphylla, such as antidiabetic, anti-inflammatory, antibacterial, antifungal, anticholinesterase, and wound-healing activity. However, T. aphylla has not received much attention for its secondary metabolites and bioactive constituents. Research has shown that this plant has hidden potential that needs to be explored. This review aims to cover botanical classification, geographical distribution, taxonomy, ethnobotanical uses, and the phytochemical compounds found in T. aphylla. The toxicology and pharmacological effects of T. aphylla are also discussed. We examined various scholarly resources to gather information on T. aphylla, including Google Scholar, Scopus, Science Direct, Springer Link, PubMed, and Web of Science. The finding of this work validates a connection between T. aphylla in conventional medicine and its antidiabetic, antibacterial, anti-inflammatory, wound-healing, antifungal, anticholinesterase, and other biological effects. T. aphylla’s entire plant (such as bark, leaves, fruits) and root extracts have been used to treat hypertension, stomach discomfort, hair loss, cough and asthma, abscesses, wounds, rheumatism, jaundice, fever, tuberculosis, and gum and tooth infection. The phytochemical screening revealed that noticeably all extracts were devoid of alkaloids, followed by the presence of tannins. In addition, different parts have revealed the existence of steroids, flavonoids, cardiac glycosides, and byproducts of gallic acid and ellagic acid. T. aphylla has shown many valuable activities against different diseases and supports its traditional uses. Therefore, high-quality preclinical research and well-designated clinical trials are needed to establish the efficacy and safety of this plant in humans.

Mechanistic target of rapamycin (mTOR) is a protein kinase that regulates cellular growth, development, survival, and metabolism through integration of diverse extracellular and intracellular stimuli. Additionally, mTOR is involved in interplay of signalling pathways that regulate apoptosis and autophagy. In cells, mTOR is assembled into two complexes, mTORC1 and mTORC2. While mTORC1 is regulated by energy consumption, protein intake, mechanical stimuli, and growth factors, mTORC2 is regulated by insulin-like growth factor-1 receptor (IGF-1R), and epidermal growth factor receptor (EGFR). mTOR signalling pathways are considered the hallmark in cancer due to their dysregulation in approximately 70% of cancers. Through downstream regulators, ribosomal protein S6 kinase β-1 (S6K1) and eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), mTORC1 influences various anabolic and catabolic processes in the cell. In recent years, several mTOR inhibitors have been developed with the aim of treating different cancers. In this review, we will explore the current developments in the mTOR signalling pathway and its importance for being targeted by various inhibitors in anti-cancer therapeutics.

Oral cancer has a high mortality rate, which is mostly determined by the stage of the disease at the time of admission. Around half of all patients with oral cancer report with advanced illness. Hitherto, chemotherapy is preferred to treat oral cancer, but the emergence of resistance to anti-cancer drugs is likely to occur after a sequence of treatments. Curcumin is renowned for its anticancer potential but its marred water solubility and poor bioavailability limit its use in treating multidrug-resistant cancers. As part of this investigation, we prepared and characterized Curcumin nanomicelles (CUR-NMs) using DSPE-PEG-2000 and evaluated the anticancer properties of cisplatin-resistant cancer cell lines. The prepared CUR-NMs were sphere-shaped and unilamellar in structure, with a size of 32.60 ± 4.2 nm. CUR-NMs exhibited high entrapment efficiency (82.2%), entrapment content (147.96 µg/mL), and a mean zeta potential of −17.5ζ which is considered moderately stable. The cellular uptake and cytotoxicity studies revealed that CUR-NMs had significantly higher cytotoxicity and cellular uptake in cisplatin drug-resistant oral cancer cell lines and parental oral cancer cells compared to plain curcumin (CUR). The DAPI and FACS analysis corroborated a high percentage of apoptotic cells with CUR-NMs (31.14%) compared to neat CUR (19.72%) treatment. Conclusively, CUR-NMs can potentially be used as an alternative carrier system to improve the therapeutic effects of curcumin in the treatment of cisplatin-resistant human oral cancer.

Alzheimer’s disease (AD) is a devastating illness with limited therapeutic interventions. The aim of this study is to investigate the pathophysiological mechanisms underlying AD and explore the potential neuroprotective effects of cocoa, either alone or in combination with other nutraceuticals, in an animal model of aluminum-induced AD. Rats were divided into nine groups: control, aluminum chloride (AlCl₃) alone, AlCl₃ with cocoa alone, AlCl₃ with vinpocetine (VIN), AlCl₃ with epigallocatechin-3-gallate (EGCG), AlCl₃ with coenzyme Q10 (CoQ10), AlCl₃ with wheatgrass (WG), AlCl₃ with vitamin (Vit) B complex, and AlCl₃ with a combination of Vit C, Vit E, and selenium (Se). The animals were treated for five weeks, and we assessed behavioral, histopathological, and biochemical changes, focusing on oxidative stress, inflammation, Wnt/GSK-3β/β-catenin signaling, ER stress, autophagy, and apoptosis. AlCl₃ administration induced oxidative stress, as evidenced by elevated levels of malondialdehyde (MDA) and downregulation of cellular antioxidants (Nrf2, HO-1, SOD, and TAC). AlCl3 also upregulated inflammatory biomarkers (TNF-α and IL-1β) and GSK-3β, leading to increased tau phosphorylation, decreased brain-derived neurotrophic factor (BDNF) expression, and downregulation of the Wnt/β-catenin pathway. Furthermore, AlCl₃ intensified C/EBP, p-PERK, GRP-78, and CHOP, indicating sustained ER stress, and decreased Beclin-1 and anti-apoptotic B-cell lymphoma 2 (Bcl-2) expressions. These alterations contributed to the observed behavioral and histological changes in the AlCl₃-induced AD model. Administration of cocoa, either alone or in combination with other nutraceuticals, particularly VIN or EGCG, demonstrated remarkable amelioration of all assessed parameters. The combination of cocoa with nutraceuticals attenuated the AD-mediated deterioration by modulating interrelated pathophysiological pathways, including inflammation, antioxidant responses, GSK-3β-Wnt/β-catenin signaling, ER stress, and apoptosis. These findings provide insights into the intricate pathogenesis of AD and highlight the neuroprotective effects of nutraceuticals through multiple signaling pathways.

Simultaneous estimation of folic acid and methotrexate in bulk and tablet dosage form by RP-HPLC-PDA was conducted via Box‒Behnken design application. Three-factor numerical values were finalized from the graphical and numerical optimization with built-in ANOVA in BBD. Sharp and symmetric peaks were observed at 4.138 and 6.929 min for folic acid and methotrexate, respectively. The mobile phase composition was methanol and 0.1% formic acid in water with a ratio of 31:69 and a flow rate of 1.1 ml/min. Both drugs were detected at a wavelength of 291 nm. The developed method was validated according to ICH guidelines. The results of the validation parameters were within acceptable limits. Stress stability studies have been performed under acidic, alkali, oxidation, neutral and photolytic conditions. Three different brand-marketed tablets were assessed with the developed method (MGXT, FOLTNAX and TRUXOFOL). In the tablet formulations, chromatogram percentages of folic acid and methotrexate were calculated at 99.13% and 99.50 in MGXT, 99.17% and 99.47 in FOLTNAX, and 99.91 and 100.05 in TRUXOFOL.