Wound healing is a complex process that can be improved through advanced biomedical approaches. Incorporating nanopolymers and plant extracts into wound dressings offers a favorable strategy for promoting tissue repair. Nanopolymers provide a controlled environment for sustained drug release while also protecting the wound from external contaminants. When combined with bioactive compounds from plant extracts, which possess antioxidant, anti-inflammatory, and antimicrobial properties, this hybrid approach can accelerate healing, reduce infection, and improve tissue regeneration. Hence, in this study, we have synthesized alginate/gelatin hydrogel blended with only nanosilver (Alg/gel-Ag) and with nanosilver and plant extracts like aloe vera, curcumin, plantain peel extract, and Calendula flower petal extract (Alg/gel-AgP). The synthesized hydrogels were characterized using different photophysical tools, and the cytotoxicity effect was studied using a fibroblast cell line (V79). The antibacterial effect of the hydrogels was also observed against E. coli and S. aureus, determining the MIC and MBC. The wound healing in vitro was also assessed using scratch assay which depicted a rapid wound closure for Alg/gel-AgP compared to the untreated control and Alg/gel-Ag. The combined effect between nanotechnology and natural extracts represents a novel and effective approach for enhancing the wound healing process.

Background/Objectives: This study explored the antitumor effect of Passiflora incarnata leaves’ nanoformulation (N-EEP) in fibroblasts, A375 cell lines, and in vivo using Dalton’s lymphoma ascites (DLA)-bearing mice. Methods: N-EEP treatment could significantly slow scratch closing in A375 cells compared to in the extract itself (EEP). Results: The hemolytic assay showed that N-EEP had less than 2% hemolysis, making the formulation highly biocompatible. In vivo N-EEP administration delayed the tumor growth rate, reduced weight gain, and increased the tumor-bearing mice’s life span. Furthermore, the ascitic cells were aspirated from the tumor and investigated for various gene expressions. The tumor suppressor gene p53, which plays a significant role in the mitochondrial-mediated apoptosis pathway, was found to be elevated in animals treated with N-EEP. We assessed the cytotoxicity of isolated DLA cells from induced mice using both the trypan blue and MTT assays, while apoptotic studies were conducted using Hoechst staining. Results from the trypan blue and MTT assays indicated that nearly 80% of the cells were killed by N-EEP treatment (200 μg/mL). Additionally, apoptosis, characterized by condensed nuclei, was observed after N-EEP treatment, confirming that one of the modes of cell death was caspase-dependent apoptosis. Conclusions: Our study suggests that N-EEP delayed the growth of DLA by upregulating p53 gene expression and inducing apoptosis.