Innate immune response induces positive inflammatory transducers and regulators in order to attack pathogens, while simultaneously negative signaling regulators are transcribed to maintain innate immune homeostasis and to avoid persistent inflammatory immune responses. The gene expression of many of these regulators is controlled by different epigenetic modifications. The remarkable impact of epigenetic changes in inducing or suppressing inflammatory signaling is being increasingly recognized. Several studies have highlighted the interplay of histone modification, DNA methylation, and post-transcriptional miRNA-mediated modifications in inflammatory diseases, and inflammation-mediated tumorigenesis. Targeting these epigenetic alterations affords the opportunity of attenuating different inflammatory dysregulations. In this regard, many studies have identified the significant anti-inflammatory properties of distinct naturally-derived phytochemicals, and revealed their regulatory capacity. In the current review, we demonstrate the signaling cascade during the immune response and the epigenetic modifications that take place during inflammation. Moreover, we also provide an updated overview of phytochemicals that target these mechanisms in macrophages and other experimental models, and go on to illustrate the effects of these phytochemicals in regulating epigenetic mechanisms and attenuating aberrant inflammation.

Cytochrome P450 (CYP450) is a group of enzymes that play an essential role in Phase I metabolism, with 57 functional genes classified into 18 families in the human genome, of which the CYP1, CYP2, and CYP3 families are prominent. Beyond drug metabolism, CYP enzymes metabolize endogenous compounds such as lipids, proteins, and hormones to maintain physiological homeostasis. Thus, dysregulation of CYP450 enzymes can lead to different endocrine disorders. Moreover, CYP450 enzymes significantly contribute to fatty acid metabolism, cholesterol synthesis, and bile acid biosynthesis, impacting cellular physiology and disease pathogenesis. Their diverse functions emphasize their therapeutic potential in managing hypercholesterolemia and neurodegenerative diseases. Additionally, CYP450 enzymes are implicated in the onset and development of illnesses such as cancer, influencing chemotherapy outcomes. Assessment of CYP450 enzyme expression and activity aids in evaluating liver health state and differentiating between liver diseases, guiding therapeutic decisions, and optimizing drug efficacy. Understanding the roles of CYP450 enzymes and the clinical effect of their genetic polymorphisms is crucial for developing personalized therapeutic strategies and enhancing drug responses in diverse patient populations.

Heavy metals like lead, mercury, cadmium, and arsenic are environmental pollutants that accumulate in ecosystems and pose significant health risks to humans and wildlife, primarily through food chain contamination where plants absorb heavy metals, affecting their growth and threatening consumer health. Cognitive and cardiovascular functions are particularly affected by exposure to heavy metals even at low concentrations through the induction of oxidative stress. Various analytical techniques are used in measuring heavy metals in different environmental and biological samples. The atomic absorption spectroscopy (AAS) offers low cost, simplicity, and portability but lacks sensitivity for certain metals. Although more sensitive, the high cost of inductively coupled plasma mass spectrometry (ICP-MS) may limit laboratory accessibility. The inductively coupled plasma with atomic emission spectrometry (ICP-AES) is known for its broad dynamic linear range and ability to identify minute variations in concentration. Atomic fluorescence spectrometry (AFS) is considered a powerful tool for quantifying heavy metals due to its high sensitivity, low detection limits, and wide linear range. The current article reviews heavy metal pollution's impact on health and spectrometric techniques for the detection of these contaminants. This may help efforts of international, and regional policies towards preventing this health hazard problem.

Non-coding RNAs (ncRNAs) have a significant role in gene regulation, especially in cancer and inflammatory diseases. ncRNAs, such as microRNA, long non-coding RNAs, and circular RNAs, alter the transcriptional, post-transcriptional, and epigenetic gene expression levels. These molecules act as biomarkers and possible therapeutic targets because aberrant ncRNA expression has been directly connected to tumor progression, metastasis, and response to therapy in cancer research. ncRNAs’ interactions with multiple cellular pathways, including MAPK, Wnt, and PI3K/AKT/mTOR, impact cellular processes like proliferation, apoptosis, and immune responses. The potential of RNA-based therapeutics, such as anti-microRNA and microRNA mimics, to restore normal gene expression is being actively studied. Additionally, the tissue-specific expression patterns of ncRNAs offer unique opportunities for targeted therapy. Specificity, stability, and immune responses are obstacles to the therapeutic use of ncRNAs; however, novel strategies, such as modified oligonucleotides and targeted delivery systems, are being developed. ncRNA profiling may result in more individualized and successful treatments as precision medicine advances, improving patient outcomes and creating early diagnosis and monitoring opportunities. The current review aims to investigate the roles of ncRNAs as potential biomarkers and therapeutic targets in cancer and inflammatory diseases, focusing on their mechanisms in gene regulation and their implications for non-invasive diagnostics and targeted therapies. A comprehensive literature review was conducted using PubMed and Google Scholar, focusing on research published between 2014 and 2025. Studies were selected based on rigorous inclusion criteria, including peer-reviewed status and relevance to ncRNA roles in cancer and inflammatory diseases. Non-English, non-peer-reviewed, and inconclusive studies were excluded. This approach ensures that the findings presented are based on high-quality and relevant sources.

This study aims to design a pH-responsive dual-loaded nanosystem based on PEGylated chitosan nanoparticles loaded with ascorbic acid (AA) and oxaliplatin (OX) for the effective treatment of breast cancer. In this regard, non-PEGylated and PEGylated chitosan nanoparticles (CS NPs) loaded with either ascorbic acid (AA), oxaliplatin (OX), or dual-loaded with AA-OX were fabricated using the ionotropic gelation method. The hydrodynamic diameters of the fabricated AA/CS NPs, OX/CS NPs, and AA-OX/CS NPs were 157.20 ± 2.40, 188.10 ± 9.70, and 261.10 ± 9.19 nm, respectively. While the hydrodynamic diameters of the designed AA/PEG-CS NPs, OX/PEG-CS NPs, and AA-OX/PEG-CS NPs were 152.20 ± 2.40, 156.60 ± 4.82, and 176.00 ± 4.21 nm, respectively. The ζ-potential of the prepared nanoparticles demonstrated high positive surface charges of +22.02 ± 1.50, +22.58 ± 1.85 and +40.4 ± 2.71 mV for AA/CS NPs, OX/CS NPs, and AA-OX/CS NPs, respectively. The ζ-potential of the PEGylated CS NPs was reduced owing to the shielding of the positive charges by the PEG chains. Additionally, all the prepared nanoparticles exhibited high entrapment efficiencies (EE%) and spherical-shaped morphology. The chemical features of the prepared nanoparticles were investigated using Fourier transform infrared (FTIR) spectroscopy. Release studies showed the capability of the prepared non-PEGylated and PEGylated chitosan NPs to release their cargo in the acidic environment of cancer tissue (pH 5.5). Furthermore, the AA/CS NPs, AA/PEG-CS NPs, OX/CS NPs, OX/PEG-CS NPs, AA-OX/CS NPs and AA-OX/PEG-CS NPs exhibited remarkable cytotoxic activities against breast adenocarcinoma (MCF-7) cells with IC₅₀ values of 44.87 ± 11.49, 23.3 ± 3.73, 23.88 ± 6.29, 17.98 ± 3.99, 18.69 ± 2.22, and 7.5 ± 0.69 µg/mL, respectively; as compared to free AA and OX (IC₅₀ of 150.80 ± 26.50 and 147.70 ± 63.91 µg/mL, respectively). Additionally, treatment of MCF-7 cells with IC₅₀ concentrations of AA, AA/CS NPs, AA/PEG-CS NPs, OX, OX/CS NPs, OX/PEG-CS NPs, AA-OX/CS NPs or AA-OX/PEG-CS NPs increased the percentages of early apoptotic cells to 5.28%, 9.53%, 11.20%, 5.27%, 13.80%, 8.43%, 2.32%, and 10.10%, respectively, and increased the percentages of late apoptotic cells to 0.98%, 0.37%, 2.41%, 2.06%, 0.97%, 9.66%, 56%, and 81.50%, respectively. These results clearly indicate that PEGylation enhances the apoptotic effect of AA and OX alone, in addition to potentiating the apoptotic effect of AA and OX when combined on MCF-7 cells. In conclusion, PEGylated chitosan nanoparticles encapsulating AA, OX, or AA and OX represent an effective formula for induction of apoptosis in MCF-7 cells.