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In this study biosynthesis approach was employed to synthesis silver nanoparticles (AgNPs) using Nigella sativa (N. sativa) seed extract (NSSE) as reducing and stabilizing agent for AgNPs. Different characterization studies confirmed successful synthesis, providing insights into their physical and chemical properties. UV–Visible spectroscopy revealed a distinct absorbance peak at 452 nm. Fourier-transform infrared spectroscopy detected the existence of various functional groups which contributed to the stabilization of the nanoparticles. X-ray diffraction indicated the crystallographic planes of the face-centered cubic (fcc) structure of AgNPs. Scanning electron microscopy illustrated a variety of polymorphic shapes in the AgNPs. Dynamic light scattering analysis determined the average size of the AgNPs to be 44.74 nm. In vitro cell culture studies demonstrated enhanced proliferation and migration of immortalized human keratinocytes cells treated with AgNPs-NSSE compared to controls. Following a 24 h of treatment, there was no apparent toxicity of AgNPs on HaCat cells. However, cell viability reached as high as 64.3 ± 0.2% at a concentration of 100 μg/mL. At a concentration of 50 μg/mL, AgNPs confirmed the capability to upregulate the expression levels of platelet-derived growth factor (50 ± 0.3%) and vascular endothelial growth factor (10 ± 0.1%) proteins in HaCat cells. These findings highlight AgNPs-NSSE as a natural and effective wound healing agent, potentially mediated through PDGF and VEGF signalling pathways. • Biosynthesis of silver nanoparticles (AgNPs) from N. sativa seeds extract (NSSE). • Comprehensive characterization methods were utilized to characterize AgNPs-NSSE. • AgNPs-NSSE has enhanced cell proliferation in HaCat cells. • AgNPs-NSSE has also improved the expression levels of PDGF and VEGF. [ABSTRACT FROM AUTHOR]

Modern lifestyle, genetics, nutritional overload through high-fat diet attributed prevalence and diabetes outcomes with various complications primarily due to obesity in which energy-dense diets frequently affect metabolic health. One possible issue usually associated with elevated chronic fat intake is insulin resistance, and hyperglycemia constitutes an important function in altering the carbohydrates and lipids metabolism. Similarly, in assessing human susceptibility to weight gain and obesity, genetic variations play a central role, contributing to keen interest in identifying the possible role of epigenetics as a mediator of gene-environmental interactions influencing the production of type 2 diabetes mellitus and its related concerns. Epigenetic modifications associated with the acceptance of a sedentary lifestyle and environmental stress factors in response to energy intake and expenditure imbalances complement genetic alterations and lead to the production and advancement of metabolic disorders such as diabetes and obesity. Methylation of DNA, histone modifications, and increases in the expression of non-coding RNAs can result in reduced transcriptional activity of key β-cell genes thus creating insulin resistance. Epigenetics contribute to changes in the expression of the underlying insulin resistance and insufficiency gene networks, along with low-grade obesity-related inflammation, increased ROS generation, and DNA damage in multiorgans. This review focused on epigenetic mechanisms and metabolic regulations associated with high-fat diet (HFD)-induced diabetes mellitus. [ABSTRACT FROM AUTHOR]