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The fabrication of zinc oxide-based nanomaterials (including natural and synthetic polymers like sulfated polysaccharide, chitosan, and polymethyl methacrylate) has potential to improve oral cancer treatment strategies. This comprehensive review explores the diverse synthesis methods employed to fabricate zinc oxide nanomaterials tailored for oral cancer applications. Several synthesis processes, particularly sol–gel, hydrothermal, and chemical vapor deposition approaches, are thoroughly studied, highlighting their advantages and limitations. The review also examines how synthesis parameters, such as precursor selection, the reaction temperature, and growth conditions, influence both the physicochemical attributes and biological efficacy of the resulting nanomaterials. Furthermore, recent advancements in surface functionalization and modification strategies targeted at improving the targeting specificity and pharmaceutical effectiveness of zinc oxide-based nanomaterials in oral cancer therapy are elucidated. Additionally, the review provides insights into the existing issues and prospective views in the field, emphasizing the need for further research to optimize synthesis methodologies and elucidate the mechanisms underlying the efficacy of zinc oxide-based nanoparticles in oral cancer therapy. [ABSTRACT FROM AUTHOR]

Globally, millions of people suffer from poor wound healing, which is associated with higher mortality rates and higher healthcare costs. There are several factors that can complicate the healing process of wounds, including inadequate conditions for cell migration, proliferation, and angiogenesis, microbial infections, and prolonged inflammatory responses. Current therapeutic methods have not yet been able to resolve several primary problems; therefore, their effectiveness is limited. As a result of their remarkable properties, bio-based materials have been demonstrated to have a significant impact on wound healing in recent years. In the wound microenvironment, bio-based materials can stimulate numerous cellular and molecular processes that may enhance healing by inhibiting the growth of pathogens, preventing inflammation, and stimulating angiogenesis, potentially converting a non-healing environment to an appropriately healing one. The aim of this present review article is to provide an overview of the mechanisms underlying wound healing and its pathophysiology. The development of bio-based nanomaterials for chronic diabetic wounds as well as novel methodologies for stimulating wound healing mechanisms are also discussed. [ABSTRACT FROM AUTHOR]

Natural products in the form of functional foods have become increasingly popular due to their protective effects against life-threatening diseases, low risk of adverse effects, affordability, and accessibility. Plant components such as phytosterol, in particular, have drawn a lot of press recently due to a link between their consumption and a modest incidence of global problems, such as Type 2 Diabetes mellitus (T2DM), cancer, and cardiovascular disease. In the management of diet-related metabolic diseases, such as T2DM and cardiovascular disorders, these plant-based functional foods and nutritional supplements have unquestionably led the market in terms of cost-effectiveness, therapeutic efficacy, and safety. Diabetes mellitus is a metabolic disorder categoriszed by high blood sugar and insulin resistance, which influence major metabolic organs, such as the liver, adipose tissue, and skeletal muscle. These chronic hyperglycemia fallouts result in decreased glucose consumption by body cells, increased fat mobilisation from fat storage cells, and protein depletion in human tissues, keeping the tissues in a state of crisis. In addition, functional foods such as phytosterols improve the body's healing process from these crises by promoting a proper physiological metabolism and cellular activities. They are plant-derived steroid molecules having structure and function similar to cholesterol, which is found in vegetables, grains, nuts, olive oil, wood pulp, legumes, cereals, and leaves, and are abundant in nature, along with phytosterol derivatives. The most copious phytosterols seen in the human diet are sitosterol, stigmasterol, and campesterol, which can be found in free form, as fatty acid/cinnamic acid esters or as glycosides processed by pancreatic enzymes. Accumulating evidence reveals that phytosterols and diets enriched with them can control glucose and lipid metabolism, as well as insulin resistance. Despite this, few studies on the advantages of sterol control in diabetes care have been published. As a basis, the primary objective of this review is to convey extensive updated information on the possibility of managing diabetes and associated complications with sterol-rich foods in molecular aspects. [ABSTRACT FROM AUTHOR]

β-sitosterol (SIT), the most abundant bioactive component of vegetable oil and other plants, is a highly potent antidiabetic drug. Our previous studies show that SIT controls hyperglycemia and insulin resistance by activating insulin receptor and glucose transporter 4 (GLUT-4) in the adipocytes of obesity induced type 2 diabetic rats. The current research was undertaken to investigate if SIT could also exert its antidiabetic effects by circumventing adipocyte induced inflammation, a key driving factor for insulin resistance in obese individuals. Effective dose of SIT (20 mg/kg b.wt) was administered orally for 30 days to high fat diet and sucrose induced type-2 diabetic rats. Metformin, the conventionally used antidiabetic drug was used as a positive control. Interestingly, SIT treatment restores the elevated serum levels of proinflammatory cytokines including leptin, resistin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) to normalcy and increases anti-inflammatory adipocytokines including adiponectin in type 2 diabetic rats. Furthermore, SIT decreases sterol regulatory element binding protein-1c (SREBP-1c) and enhances Peroxisome Proliferator–activated receptor-γ (PPAR-γ) gene expression in adipocytes of diabetic rats. The gene and protein expression of c-Jun-N-terminal kinase-1 (JNK1), inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ) and nuclear factor kappa B (NF-κB) were also significantly attenuated in SIT treated groups. More importantly, SIT acts very effectively as metformin to circumvent inflammation and insulin resistance in diabetic rats. Our results clearly show that SIT inhibits obesity induced insulin resistance by ameliorating the inflammatory events in the adipose tissue through the downregulation of IKKβ/NF-κB and c-Jun-N-terminal kinase (JNK) signaling pathway. [ABSTRACT FROM AUTHOR]