The green synthesis of inorganic nanoparticles (NPs) using bio-materials has attained enormous attention in recent years due to its simple, eco-friendly, low-cost and non-toxic nature. In this work, silver nanoparticles (AgNPs) and gold nanoparticles (AuNPs) were synthesized by the marine algae extract, Sargassum serratifolium (SS). The characteristic studies of bio-synthesized SS-AgNPs and SS-AuNPs were carried out by using ultraviolet–visible (UV–Vis) absorption spectroscopy, dynamic light scattering (DLS), high-resolution transmission electron microscope (HR-TEM), selected area electron diffraction (SAED), energy-dispersive X-ray spectroscopy (EDX), X-ray powder diffraction (XRD) and Fourier transform infrared spectroscopy (FT-IR). Phytochemicals in the algae extract, such as meroterpenoids, acted as a capping agent for the NPs’ growth. The synthesized Ag and Au NPs were found to have important catalytic activity for the degradation of organic dyes, including methylene blue, rhodamine B and methyl orange. The reduction of dyes by SS-AgNPs and -AuNPs followed the pseudo-first order kinetics.

Background: Combination therapy remains a promising strategy for treating neurodegenerative diseases, although green synthesis of gold nanoparticles for treating chronic neuroinflammation and studying their efficacy in treating neuroinflammation-mediated neurodegenerative diseases is not well assessed. Results: Here, Ephedra sinica Stapf (ES) extract was used as the reducing, capping, and stabilizing agent for gold nanoparticle synthesis. We developed ES extract-capped gold nanoparticles (ES-GNs) and investigated their anti-neuroinflammatory properties in microglia. ES-GNs displayed maximum absorption at 538 nm in ultraviolet-visible spectroscopy. Dynamic light scattering assessment revealed that ES-GN diameter was 57.6±3.07 nm, with zeta potential value of −24.6±0.84 mV. High resolution–transmission electron microscopy confirmed the spherical shape and average diameter (35.04±4.02 nm) of ES-GNs. Crystalline structure of ES-GNs in optimal conditions was determined by X-ray powder diffraction, and elemental gold presence was confirmed by energy-dispersive X-ray spectroscopy. Fourier transform-infrared spectroscopy confirmed gold nanoparticle synthesis using ES. Anti-neuroinflammatory properties of ES-GNs on production of pro-inflammatory mediators (nitric oxide, prostaglandin E₂, and reactive oxygen species) and cytokines (tumor necrosis factor-α, IL-1β, and IL-6) in lipopolysaccharide (LPS)-stimulated microglia were investigated by ELISA and flow cytometry. ES-GNs significantly attenuated LPS-induced production of pro-inflammatory mediators and cytokines, which was related to suppressed transcription and translation of inducible nitric oxide synthase and cyclooxygenase-2, determined by RT-PCR and western blotting. ES-GNs downregulated upstream signaling pathways (IκB kinase-α/β, nuclear factor-κB, Janus-activated kinase /signal transducers and activators of transcription, mitogen-activated protein kinase , and phospholipase D) of pro-inflammatory mediators and cytokines in LPS-stimulated microglia. Anti-neuroinflammatory properties of ES-GNs were mediated by ES-GNs-induced AMP-activated protein kinase)-mediated nuclear erythroid 2-related factor 2 /antioxidant response element signaling. Conclusion: Collectively, these findings provide a new insight on the role of ES-GNs in treating chronic neuroinflammation-induced neurodegenerative diseases.

Oxidative stress‑induced cellular senescence is an important contributor to the pathogenesis of age‑related macular degeneration (AMD). Characteristics of premature cellular senescence include a loss of proliferation, change in cell shape, irreversible cell cycle arrest, and elevated senescence‑associated β‑galactosidase (SA‑β‑gal) activity. It was hypothesized that lutein may have anti‑senescence potential and may be useful as a treatment for AMD. In the present study, premature cellular senescence was induced in ARPE‑19 cells via treatment with H2O2 and the effects of lutein application were confirmed by observing cell morphology, lysosome contents, reactive oxygen species (ROS) generation and SA‑β‑gal activity, and cell cycle progression. The protein expression was also analyzed via western blotting in order to identify the affected signaling pathways. The results revealed that H2O2 treatment induced premature cellular senescence in ARPE‑19 cells, as evidenced by an increased production of ROS and SA‑β‑gal, altered lysosome contents, changed cellular morphology and arrested cell cycle progression. However, when treated with lutein, ARPE‑19 cells were effectively protected from these H2O2‑induced effects. Western blot analysis revealed that lutein induced the expression of heme oxygenase‑1, NAD(P)H quinone dehydrogenase 1, sirtuin (SIRT)‑1, and SIRT3. Together, the results indicated that lutein protects cells from cellular senescence induced by oxidative stress; therefore, it may be able to suppress the progression of AMD. In addition, our increased understanding of the pathways through which lutein acts is useful for the development of novel therapies for the treatment of oxidative stress‑associated retinal disease.

The effect of gold nanoparticles (GNPs) synthesized in marine algae has been described in the context of skin, where they have shown potential benefit. Ecklonia stolonifera (ES) is a brown algae that belongs to the Laminariaceae family, and is widely used as a component of food and medicine due to its biological activities. However, the role of GNPs underlying cellular senescence in the protection of Ecklonia stolonifera gold nanoparticles (ES-GNPs) against UVA irradiation is less well known. Here, we investigate the antisenescence effect of ES-GNPs and the underlying mechanism in UVA-irradiated human dermal fibroblasts (HDFs). The DPPH and ABTS radical scavenging activity of ES extracts was analyzed. These analyses showed that ES extract has potent antioxidant properties. The facile and optimum synthesis of ES-GNPs was established using UV-vis spectra. The surface morphology and crystallinity of ES-GNPs were demonstrated using high resolution transmission electron microscopy (HR-TEM), energy dispersive spectroscopy (EDS), X-ray diffraction (XRD), and Fourier-transform infrared spectroscopy (FT-IR). ES-GNPs presented excellent photocatalytic activity, as shown by the photo-degradation of methylene blue and rhodamine B. A cellular senescence model was established by irradiating HDFs with UVA. UVA-irradiated HDFs exhibited increased expression of senescence-associated β-galactosidase (SA-β-galactosidase). However, pretreatment with ES-GNPs resulted in reduced SA-β-galactosidase activity in UVA-irradiated HDFs. Intracellular ROS levels and G1 arrest in UVA-irradiated HDFs were checked against the background of ES-GNP treatment to investigate the antisenescence effects of ES-GNPs. The results showed that ES-GNPs significantly inhibit UVA-induced ROS levels and G1 arrest. Importantly, ES-GNPs significantly downregulated the transcription and translation of MMP (matrix metalloproteinases)-1/-3, which regulate cellular senescence in UVA-irradiated HDFs. These findings indicate that our optimal ES-GNPs exerted an antisenescence effect on UVA-irradiated HDFs by inhibiting MMP-1/-3 expression. Collectively, we posit that ES-GNPs may potentially be used to treat photoaging of the skin.