Ahram Canadian University

This comprehensive review presents a thorough examination of recent advances in nanoemulsion (NE) green technology, focusing on biomass-assisted synthesis, characterization, and the diverse biomedical implications of these nanoscale emulsions. NEs, characterized by their minute droplet sizes and kinetic stability, have garnered considerable attention due to their potential applications across various biomedical fields. This review presents a comprehensive analysis of state-of-the-art synthesis methods, including mini-emulsion polymerization, NE–solvent evaporation, spontaneous emulsification, sol–gel techniques, and innovative strategies for producing complex multicomponent materials. Emphasis is placed on the evolution of synthetic approaches, offering insights into the current landscape of NE production. In exploring the biomedical applications, the study categorizes nanocarriers formed within NEs, distinguishing between polymeric, inorganic, and hybrid nanocarriers based on their chemical composition. Noteworthy advancements in synthetic strategies are outlined for each category, showcasing the dynamic nature of NEs technology. A key highlight is the discussion of emerging trends in biomedical applications, spanning medicine, food, agriculture, cosmetics, and environmental science. Specific attention is given to the role of NEs in nanofiltration, elucidating their effectiveness in removing diverse pharmaceuticals through polyamide nano-filters. Moreover, the manuscript delves into the pivotal role of NEs in bioremediation, addressing hazardous substances such as PFASs through adsorption, photo-degradation/defluorination, and other innovative mechanisms. This review aims to provide a contemporary overview of green NE technologies, offering valuable insights for researchers, scientists, and practitioners in nanotechnology, pharmaceuticals, and biomedical sciences.

Ischemic acute kidney injury (AKI) remains a major clinical challenge, characterized by high morbidity, mortality, and a substantial risk of progression to chronic kidney disease. Accumulating evidence indicates that ischemic AKI is not merely a transient hemodynamic disorder but a complex, biologically orchestrated process driven by microvascular dysfunction, innate immune activation, inflammatory signaling, and maladaptive tissue repair. Despite advances in supportive care, effective disease-modifying therapies are still lacking. Recent studies have highlighted that key signaling pathways, including Toll-like receptor/nuclear factor-κB (TLR/NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), purinergic P2X7 receptor–inflammasome signaling, heat-shock protein–mediated stress responses, and phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) cascades, govern the initiation, amplification, and resolution of ischemic renal injury. These pathways converge on downstream cellular effectors such as cell adhesion molecules (CAMs), which orchestrate leukocyte recruitment, endothelial-epithelial interactions, and spatial propagation of inflammation within the renal microvasculature. Natural compounds have emerged as promising therapeutic candidates for ischemic AKI due to their pleiotropic pharmacological properties and ability to modulate multiple pathogenic signaling networks simultaneously. A growing body of experimental evidence demonstrates that polyphenols, glycosides, saponins, and related phytochemicals attenuate ischemic renal injury by suppressing inflammatory signaling, reducing CAM expression, preserving microcirculatory integrity, and promoting adaptive repair. Furthermore, advances in nanocarrier-based delivery systems have substantially enhanced the translational potential of these compounds by improving bioavailability, renal targeting, and pathway-specific modulation. In this review, we provide a comprehensive, signaling-centered analysis of ischemic AKI pathogenesis and systematically map natural compounds to their molecular targets and downstream inflammatory effectors. By integrating mechanistic insights with emerging nanotherapeutic strategies, this work offers a structured framework for the rational development of multi-target, mechanism-based interventions for ischemic AKI. It highlights key challenges and future directions for clinical translation.

Baicalin, a polyphenolic flavonoid, is the main bioactive flavone extracted from the roots of Scutellaria baicalensis. It has received increasing interest due to its broad spectrum of pharmacological activities and therapeutic benefits demonstrated in preclinical research. However, its molecular mechanisms and translational potential remain underdefined. This review systematically evaluates current evidence on baicalin, including its natural sources, chemical structure, biosynthesis, extraction techniques, pharmacokinetic features, molecular mechanisms, and therapeutic applications, as well as developments in drug delivery platforms designed to overcome its biopharmaceutical limitations. This structured literature review was conducted using data extracted from various databases, including the Egyptian Knowledge Bank, Scopus, Web of Science, PubMed, Google Scholar, and Elsevier. All possible keywords relevant to baicalin were utilized. Recent original articles, systematic reviews, meta-analysis, clinical studies, and high-quality reviews were prioritized. Baicalin exerts its therapeutic effects through modulation of various signaling pathways, primarily involving oxidative stress and inflammation. It exhibits anticancer, antimicrobial, antiviral, immunomodulatory, metabolic, and dermatological effects and alleviates various system disorders and drug-induced toxicity. Despite promising preclinical data, clinical translation is hindered by its poor solubility, limited bioavailability, and insufficient clinical validation. Emerging nano-delivery systems, such as liposomes, solid lipid nanoparticles, polymeric nanoparticles, and surface-modified nanoplatforms, have greatly improved the pharmacokinetic performance of baicalin. Nevertheless, the clinical translation of these approaches remains limited. While baicalin represents a promising multi-target therapeutic option, substantial research gaps remain. Future research should give priority to deeper mechanistic investigations, standardized formulation approaches, and well-designed clinical trials to bridge the gap between preclinical efficacy and clinical application, and to establish its optimal dosing, safety profile, and long-term efficacy.

Alzheimer disease (AD) is the most common cause of dementia in the world with the prevalence expected to increase threefold to 152.8 million people by 2050. The current medications provide a short-term ameliorative effect, and this requires development of disease-modifying treatments, which address the biological pathogenesis. This review assesses the changing neuropharmacological environment offering a critical analysis of anti-amyloid monoclonal antibodies and investigates the so-called expanding frontier of non-amyloid targets. It also examines the approaches of clinical trials and the trend of biomarker-based patient selection and precision medicine. Although β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. Nevertheless, the treatments are associated with amyloid-related imaging abnormalities (ARIA). In addition to amyloid, studies are focusing on tau hyperphosphorylation, neuroinflammation through triggering receptor on myeloid cells 2 (TREM2) and NLR family pyrin domain containing 3 (NLRP3) and growth factor-mediated synaptic plasticity through brain-derived neurotrophic factor (BDNF). AD treatment has entered the new era that demands a paradigm shift from monotherapies to multi-target cocktails. The future lies in precision neuropharmacology, where genetic stratification and individual biomarker analysis are used to provide the correct treatment at the most appropriate biological stage.

This study evaluates the protective potential of Fondaparinux (Fond), a selective antithrombin-mediated Factor Xa inhibitor, in methotrexate-induced hepatotoxicity. The work explores its ability to correct coagulation imbalance, improve endothelial function, and attenuate oxidative and inflammatory cascades (TLR4/NLRP3, NF-κB p65/IL-1β/MCP-1). Animals were allocated into 4 groups. A control group was given distilled water via the intraperitoneal route (i.p.); an MTX group was given a single intraperitoneal injection of MTX (20 mg/kg) on the seventh experimental day; and two groups received prior prophylactic administration of Fondaparinux (at doses of 5 or 10 mg/kg, intraperitoneally) throughout seven consecutive days before as well as for an additional four-day period following MTX administration. MTX significantly elevated hepatic injury markers (AST, ALT, ALP), induced oxidative stress with depleted antioxidants (SOD, GSH), and activated TLR4/NLRP3 signaling, resulting in upregulation of inflammatory mediators (TNF-α, NF-κB p65, IL-18, IL-1β, MCP-1, caspase-1, iNOS, ICAM-1, MPO) and suppression of IL-10 (p < 0.05). Endothelial dysfunction was evidenced by reduced eNOS. MTX also triggered marked coagulation disturbances, including enhanced Factor Xa–dependent thrombin generation, increased tissue factor, fibrin deposition, and elevated PAI-1. Mitochondrial apoptotic signaling was promoted, as indicated by elevated expression of cytochrome c along with induced caspase-3 and caspase-9 activation . Histologically, MTX caused extensive hepatic damage characterized by periportal fibrosis, inflammatory infiltration, bile duct proliferation, hepatocellular necrosis, vacuolation, and vascular congestion. Fondaparinux pretreatment dose-dependently restored hemostatic balance, improved endothelial function, suppressed oxidative and inflammatory responses, attenuated apoptosis, and markedly ameliorated histopathological alterations. Fondaparinux limits methotrexate-associated liver damage through inhibition of Factor Xa–dependent coagulation pathways while providing antioxidant, anti-inflammatory, anti-apoptotic, and hepatoprotective actions.