Cinnamomum verum plant extract mediated propellant chemistry route was used for the green synthesis of zinc oxide nanoparticles. Prepared samples were confirmed for their nano regime using advanced characterization techniques such as powder X-ray diffraction and microscopic techniques such as scanning electron microscopy and transmission electron microscopy. The energy band gap of the green synthesized zinc oxide (ZnO)-nanoparticles (NPs) were found between 3.25–3.28 eV. Fourier transmission infrared spectroscopy shows the presence of Zn-O bond within the wave number of 500 cm⁻¹. SEM images show the specific agglomeration of particles which was also confirmed by TEM studies. The green synthesized ZnO-NPs inhibited the growth of Escherichia coli and Staphylococcus aureus with a minimum inhibitory concentration (MIC) of 125 µg mL⁻¹ and 62.5 µg mL⁻¹, respectively. The results indicate the prepared ZnO-NPs can be used as a potential antimicrobial agent against harmful pathogens.

Cerium oxide nanoparticles (CeO₂NPs) have a broad scale of applications in the biomedical field due to their excellent physicochemical and catalytic properties. The present study aims to synthesize the CeO₂NPs from Centella asiatica (C. asiatica) leaf extract, which has been used in Indian traditional medicine for its neuroprotective properties. The CeO₂NPs were characterized by ultraviolet-visible, X-ray diffraction, Fourier transform infrared, Raman spectroscopy, scanning electron microscopy- energy dispersive X-ray spectroscopy, and high-resolution transmission electron microscopy. The antioxidant property was evaluated by 2,2-di (4-tert-octyl phenyl)-1-picrylhydrazyl and OH radical assays. The neuroprotective potential was assessed against the oxidative stress (OS) induced by H₂O₂ in the human neuroblastoma (SH-SY5Y) cell line. CeO₂NPs exhibited significant DPPH and OH radical scavenging activity. Our results revealed that CeO₂NPs significantly increased H₂O₂-induced cell viability, decreased lactate dehydrogenase, protein carbonyls, reactive oxygen species generation, apoptosis, and upregulated antioxidant enzyme activity. Our findings suggest that the CeO₂NPs protect the SH-SY5Y cells from OS and apoptosis, which could potentially counter OS-related neurodegenerative disorders.

The development of advanced glycation end-products (AGEs) inhibitors is considered to have therapeutic potential in diabetic complications inhibiting the loss of the biomolecular function. In the present study, zinc oxide nanoparticles (ZnO-NPs) were synthesized from aqueous leaf extract of Morus indica and were characterized by various techniques such as ultraviolet (UV)-Vis spectroscopy, Powder X-Ray Diffraction (PXRD), Fourier Transform Infrared Spectroscopy (FT-IR), Scanning electron microscopy (SEM), and energy dispersive spectroscopy (EDS). Further, the inhibition of AGEs formation after exposure to ZnO-NPs was investigated by in-vitro, in-vivo, and molecular docking studies. Biochemical and histopathological changes after exposure to ZnO-NPs were also studied in streptozotocin-induced diabetic rats. ZnO-NPs showed an absorption peak at 359 nm with a purity of 92.62% and ~6–12 nm in size, which is characteristic of nanoparticles. The images of SEM showed agglomeration of smaller ZnO-NPs and EDS authenticating that the synthesized nanoparticles were without impurities. The biosynthesized ZnO-NPs showed significant inhibition in the formation of AGEs. The particles were effective against methylglyoxal (MGO) mediated glycation of bovine serum albumin (BSA) by inhibiting the formation of AGEs, which was dose-dependent. Further, the presence of MGO resulted in complete damage of biconcave red blood corpuscles (RBCs) to an irregular shape, whereas the morphological changes were prevented when they were treated with ZnO-NPs leading to the prevention of complications caused due to glycation. The administration of ZnO-NPs (100 mg Kg⁻¹) in streptozotocin(STZ)-induced diabetic rats reversed hyperglycemia and significantly improved hepatic enzymes level and renal functionality, also the histopathological studies revealed restoration of kidney and liver damage nearer to normal conditions. Molecular docking of BSA with ZnO-NPs confirms that masking of lysine and arginine residues is one of the possible mechanisms responsible for the potent antiglycation activity of ZnO-NPs. The findings strongly suggest scope for exploring the therapeutic potential of diabetes-related complications.

Purpose: 4-Hydroxyisophthalic acid (4-HIA) is a bioactive compound present in the roots of Decalepis hamiltonii, which has attracted considerable attention in attenuating oxidative stress-related neurodegenerative diseases. However, its efficacy is limited because of its low solubility and bioavailability. Therefore, the present study aimed to encapsulate 4-HIA using biocompatible copolymer polylactide-co-glycolide (PLGA) and evaluate its antioxidant and neuroprotective potential. Methods: The nanoparticles (NPs) were fabricated by solid/oil/water (s/o/w) emulsion technique and characterized using XRD, SEM, HR-TEM, and FTIR spectroscopy. Antioxidant assays such as 1,1 diphenyl-2-picrylhydrazyl (DPPH), superoxide, and hydroxyl radical scavenging ability were performed to assess the antioxidant potential of the fabricated NPs. Results: The bioactive component, 4-HIA, was efficiently encapsulated by the PLGA polymer and was found to be spherical and smooth with a size < 10nm. 4-HIA showed better scavenging capability in DPPH and superoxide assays as compared to 4-HIA encapsulated PLGA and butylated hydroxytoluene (BHT). In contrast, 4-HIA encapsulated PLGA NPs exhibited a significant hydroxyl radical scavenging activity than 4-HIA and BHT alone. Further, the encapsulated NPs efficiently curtailed hydrogen peroxide (H₂O₂)-induced cytotoxicity in PC12 cells. Conclusion: Our findings indicate that 4-HIA encapsulated PLGA NPs might be a therapeutic intervention towards the effective management of oxidative stress as it has exhibited efficient neuroprotective potential against H₂O₂-induced oxidative stress in PC12 cells.