Green synthesis is a new paradigm for the preparation of gold nanoparticles (AuNPs) due to its cost-effectiveness and favorable environmental impact. This study presented a simple phytosynthesis process for the preparation of AuNPs utilizing the aqueous peel extract of Spondias dulcis (SPE) (Anacardiaceae) as both a reducing and stabilizing agent. A visual color change from yellow to purple during the reaction implied the successful formation of SPE-AuNPs, which was confirmed by UV–vis spectroscopy. Transmission electron microscopy (TEM) images indicated that the SPE-AuNPs were predominantly spherical with a mean size of 36.75 ± 11.36 nm, and were comprised of crystalline Au, as indicated by X-ray diffraction. In terms of their potential application, SPE-AuNPs exhibit significant cytotoxic activity in a dose- and time-dependent manner to MCF-7 human breast cancer cells, while being non-toxic to Vero normal cells. The treatment of MCF-7 cells with SPE-AuNPs increased the production of intracellular reactive oxygen species (ROS). Herein, the findings highlight the potential contribution of phytosynthesized SPE-AuNPs to the development of novel nanomedicines for cancer treatment.

Cholangiocarcinoma (CCA) is a rare malignancy of the biliary tract with extremely poor clinical outcomes due to a lack of effective therapies to improve disease management. The emerging green synthesis of gold nanoparticles (AuNPs) has extensively provided their use in biomedical applications. In this study, we developed AuNPs via reducing gold salts with apigenin (4′,5,7-trihydroxyflavone). The synthesized apigenin-conjugated AuNPs (api-AuNPs) were physicochemically characterized by various techniques before evaluation their biological and functional inhibition in a CCA cell line, KKU-M055. The mean size of api-AuNPs was 90.34 ± 22.82 nm with zeta potential of -36 ± 0.55. The half-maximal inhibitory concentration (IC₅₀, 0.8 mg/mL) of api-AuNPs on cell proliferation of KKU-M055 was 1.9-fold less than that of an immortalized human cholangiocyte cell line, MMNK1 (IC₅₀, 1.5 mg/mL). Moreover, api-AuNPs induced cell apoptosis via the up-regulation of Bax, Bid, and Caspase 3, and down-regulation of Bcl2, leading to elevated caspase 3/7, 8, 9 activities and reactive oxygen species (ROS) production. The api-AuNPs significantly inhibited the migration of KKU-M055 cells and suppressed the proliferation, migration, and in vitro tube formation of vascular endothelial cells. Collectively, our findings indicate the dual abilities of api-AuNPs that potentially inhibit cancer cell growth and motility as well as endothelial cell-mediated angiogenesis, which may offer a novel therapeutic avenue to treat CCA patients effectively.

Chitosan-based scaffolding possesses unique properties that make it highly suitable for tissue engineering applications. Chitosan is derived from deacetylating chitin, which is particularly abundant in the shells of crustaceans. This study aimed to extract chitosan from shrimp shell waste (Macrobrachium rosenbergii) and produce biocomposite scaffolds using the extracted chitosan for cartilage tissue engineering applications. Chitinous material from shrimp shell waste was deproteinized and deacetylated. The extracted chitosan was characterized and compared to commercial chitosan through various physicochemical analyses. The findings revealed that the extracted chitosan shares similar trends in the Fourier transform infrared spectroscopy spectrum, energy dispersive X-ray mapping, and X-ray diffraction pattern to commercial chitosan. Despite differences in the degree of deacetylation, these results underscore its comparable quality. The extracted chitosan was mixed with agarose, collagen, and gelatin to produce the blending biocomposite AG-CH-COL-GEL scaffold by freeze-drying method. Results showed AG-CH-COL-GEL scaffolds have a 3D interconnected porous structure with pore size 88-278 μm, high water uptake capacity (>90%), and degradation percentages in 21 days between 5.08% and 30.29%. Mechanical compression testing revealed that the elastic modulus of AG-CH-COL-GEL scaffolds ranged from 44.91 to 201.77 KPa. Moreover, AG-CH-COL-GEL scaffolds have shown significant potential in effectively inducing human chondrocyte proliferation and enhancing aggrecan gene expression. In conclusion, AG-CH-COL-GEL scaffolds emerge as promising candidates for cartilage tissue engineering with their optimal physical properties and excellent biocompatibility. This study highlights the potential of using waste-derived chitosan and opens new avenues for sustainable and effective tissue engineering solutions_.

Colorectal carcinoma (CRC) is one of the most common malignancies, though there are no effective therapeutic regimens at present. This study aimed to investigate the inhibitory effects of mannooligosaccharides extracted from coconut meal (CMOSs) on the proliferation and migration of human colorectal cancer HCT116 cells in vitro. The results showed that CMOSs exhibited significant inhibitory activity against HCT116 cell proliferation in a concentration-dependent manner with less cytotoxic effects on the Vero normal cells. CMOSs displayed the ability to increase the activation of caspase-8, –9, and –3/7, as well as the generation of reactive oxygen species (ROS). Moreover, CMOSs suppressed HCT116 cell migration in vitro. Interestingly, treatment of human microvascular endothelial cells (HMVECs) with CMOSs resulted in the inhibition of cell proliferation, cell migration, and capillary-like tube formation, suggesting its anti-vascular angiogenesis. In summary, the results of this study indicate that CMOSs could be a valuable therapeutic candidate for CRC treatment.

Cholangiocarcinoma (CCA) is a rare and highly aggressive cancer of the biliary tract, associated with poor clinical outcomes due to late diagnosis, extensive metastasis, drug resistance, and limited treatment options. Apigenin, a natural flavonoid, has been found to exhibit anticancer properties in several types of human cancer cells. Therefore, apigenin may be relevant to developing chemotherapeutic agents for cancer treatment. In this study, we examined the effects of apigenin on cell viability, cell cycle distribution, apoptosis, and cell migration in human CCA cell lines (KKU-M055) under in vitro conditions. The results demonstrate that apigenin significantly suppressed specific CCA cell proliferation by inducing cell cycle arrest at the G2/M phase and promoting cell apoptosis in KKU-M055 cells while exhibiting low toxicity in immortalized MMNK1 cells. Apigenin enhanced apoptotic features, including nuclear fragmentation and the loss of mitochondrial membrane potential. Furthermore, apigenin induced the apoptosis of KKU-M055 cells in both extrinsic and intrinsic pathways by activating caspase-8, -9, and -3/7. Moreover, apigenin inhibited KKU-M055 migration. Our study suggests apigenin as a promising candidate for treating CCA, and these findings provide theoretical support for the further development and potential application of apigenin in clinical CCA therapy.