Withaferin A (WA), a bioactive compound derived from the Ashwagandha plant, has been recognized for its anticancer properties. We tested various concentrations of WA, Fluvastatin (FLU), and their combinations (ranging from 0 to 160 µM) for their potential regulatory effects on colon cancer cells (Caco-2 cell line) and non-tumorigenic colon cells (NCM-460). Our results showed that at lower concentrations (around10 µM), WA significantly impacted colon cancer cells, showing minimal toxicity to normal cells (NCM-460). However, at higher concentrations, FLU selectively inhibited cancer cell proliferation, with noticeable toxicity to both cancerous and normal cells. Additionally, WA treatment led to a time and dose-dependent decrease in the production of IL-1β and TNF-α. Along with these effects, the downregulation of ERK and EGF gene expression was observed across all treatments. Additionally, docking analysis revealed the potential regulatory role of WA and its interaction with aspartate aminotransferase, in comparison to the docking data for FLU, which serves as a standard inhibitor for aspartate aminotransferase. These findings suggest that WA can inhibit cell proliferation signaling by targeting ERK and EGF, thereby promoting programmed cell death (PCD) in treated cells. These data also demonstrate that WA, whether alone or in combination with other compounds, can regulate the production of pro-inflammatory cytokines in treated cells.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, characterized by progressive cognitive decline, memory impairment, and behavioral dysfunction. Despite extensive research, effective disease-modifying therapies remain limited, largely due to incomplete understanding of its complex and multifactorial pathogenesis. Increasing evidence now highlights chronic neuroinflammation as a central contributor to AD progression, shifting focus from a purely proteinopathy-based model toward an integrated neuroimmune perspective. Among key inflammatory pathways, the NLRP3 inflammasome has emerged as a critical innate immune signaling platform that links pathological protein aggregation to sustained neuroinflammatory responses in the central nervous system. Activation of the NLRP3 inflammasome is triggered by multiple Alzheimer’s disease–associated pathological stimuli, including amyloid-β accumulation, tau pathology, autophagy dysfunction, mitochondrial impairment, oxidative stress, and endoplasmic reticulum stress. These cellular disturbances converge to promote assembly of the inflammasome complex and activation of caspase-1. Activated caspase-1 mediates the proteolytic maturation and release of the pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18), both of which play central roles in amplifying neuroinflammatory signaling, promoting synaptic dysfunction, and contributing to neuronal injury. Consequently, IL-1β and IL-18 have gained increasing attention as potential biomarkers for disease severity, progression, and inflammatory burden in Alzheimer’s disease. In addition, inflammasome-specific markers such as apoptosis-associated speck-like protein containing CARD (ASC) specks provide further mechanistic and diagnostic evidence of active inflammasome signaling in neurodegeneration. Preclinical studies using cellular and animal models have demonstrated that pharmacological inhibition of the NLRP3 inflammasome can reduce neuroinflammation, attenuate neuropathological changes, and improve cognitive performance. However, despite these promising findings, clinical translation remains limited due to challenges including inadequate blood–brain barrier penetration, systemic immune modulation risks, and the absence of reliable biomarker-guided patient stratification strategies. This review critically examines the molecular mechanisms underlying NLRP3 inflammasome activation in Alzheimer’s disease, its interaction with pro-inflammatory cytokine networks, and the emerging role of inflammasome-related biomarkers in disease characterization. Furthermore, current therapeutic strategies targeting the NLRP3 pathway are discussed, along with key translational barriers and future directions for developing biomarker-driven immunomodulatory therapies in Alzheimer’s disease.

Sugarcane (Saccharum officinarum) is a highly efficient agro-industry plant with known ability to accumulate biomass and produce sucrose sugar, making it an essential cash crop globally. This also results in the environmental pollution due to the accumulation of sugarcane biomass, the plant residues. left behind after extraction of sugar. This study was conducted to determine the phytochemicals contents, proximate, mineral, and antioxidant activities of sugarcane and its biomass, with a focus on their sustainable utilization through agricultural, therapeutic and industrial application. The samples were collected from Sharada market, Kano State, Nigeria, and analyzed for phytochemical using quantitative and qualitative method and antioxidant activities using the (DPPH, FRAP) method, proximate using standard Association of Analytical Chemistry (AOAC) methods and mineral using the Atomic Absorption Spectroscopy (AAS).The results revealed that sugarcane biomass had higher fiber and carbohydrate content (26.01±0.02% and 79.34±6.96%, respectively) compared to raw sugarcane (19.19±0.02% and 62.75±0.96%). However, sugarcane had a higher moisture (2.41±0.34%), fat (1.52±0.64%), and protein content (0.42±0.01%) than the biomass. In terms of mineral composition, sugarcane exhibited higher iron (5.59±0.17 mg/l), manganese (0.20±0.002 mg/l), and calcium concentration (14.10±0.03mg/l), while the biomass contained more potassium (207.5±0.24 mg/l). The result revealed that sugarcane had higher total phenolic content (279.92±3.66), compared to sugarcane biomass (255.65±9.48), also contains higher total flavonoids content (95.90±2.04) compared to sugarcane biomass (88.79±1.33). However, sugarcane had a higher antioxidant activity in term of the DPPH assay with an IC50 value of (774.28±5.60) higher than the biomass which has (1234.64±8.03). In terms of Ferric reducing antioxidant power (FRAP) Sugarcane exhibited higher antioxidant activity at higher concentration while the biomass shows higher antioxidant activity at low concentration. Sugarcane and sugarcane biomass has strong antioxidant activity, this indicate that the sugarcane and sugarcane biomass are effective in giving antioxidant protection at various levels, inhibition of radical formation (by reducing iron complexes). These findings suggest that sugarcane and sugarcane biomass are richer in phytochemicals which makes it suitable for the treatment of several ailments. Also, that sugarcane is nutritionally richer in proteins and essential trace minerals, whereas the biomass is an excellent source of dietary fiber and macro minerals, making it suitable for bio-fuel production, animal feed, and soil enrichment. The utilization of sugarcane biomass as a renewable resource could alleviate environmental pollution caused by waste disposal while promoting sustainable agriculture and energy solutions. Therefore, utilizing the full potential of sugarcane