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Amyloid β (Aβ) plaque accumulation‐mediated neuronal toxicity has been suggested to cause synaptic damage and consequent degeneration of brain cells in Alzheimer's disease (AD). With the increasing prerequisite of eco‐friendly nanoparticles (NPs), research investigators are utilizing green approaches for the synthesis of zinc oxide (ZnO) NPs for pharmaceutical applications. In this present study, ZnO NPs were synthesized from Acanthus ilicifolius to assess the neuroprotective properties in the AD model of transgenic Caenorhabditis elegans strains CL2006 and CL4176 expressing Aβ aggregation. Our findings revealed that the therapeutic effect of green‐synthesized ZnO NPs is associated with antioxidant activity. We also found that ZnO NPs significantly enhance the C. elegan's lifespan, locomotion, pharyngeal pumping, chemotaxis behavior also diminish the ROS deposition and intracellular productionMoreover, thioflavin T staining demonstrated that ZnO NPs substantially attenuated the Aβ deposition in the C. elegans strain as compared to untreated worms. With their antioxidant properties, the greenly synthesized ZnO NPs had a significant neuroprotective efficiency on Aβ‐induced toxicity by reducing Aβ aggregation and specifically reducing the progression of paralysis in the C. elegans AD model. Our findings suggested that the biosynthesized ZnO NPs could be thought‐provoking candidates for age‐associated neurodegenerative disorders accompanied by oxidative stress. [ABSTRACT FROM AUTHOR]

In this study, we prepared ferulic acid (FA) and paclitaxel (PTX) co‐loaded polyamidoamine (PAMAM) dendrimers conjugated with arginyl–glycyl–aspartic acid (RGD) to overcome P‐glycoprotein (P‐gp)‐mediated multidrug resistance (MDR). FA was released in greater extent (80%) from the outer layer of the dendrimers compared with PTX (70%) from the interior of the dendrimers. FA improved intracellular availability of PTX via P‐gp modulation in drug‐resistant cells. In vitro drug uptake data show higher PTX delivery with RGD–PAMAM–FP than with PAMAM–FP in drug resistant KB CH‐R 8‐5 cell lines. This indicates that RGD facilitates intracellular PTX accumulation through active targeting in multidrug‐resistant KB CH‐R 8‐5 cells. The terminal deoxynucleotidyl transferase 2ʹ‐deoxyuridine 5ʹ‐triphosphate nick‐end labeling assay data and membrane potential analysis in mitochondria confirm the enhanced anticancer potential of RGD–PAMAM–FP nanoaggregates in drug‐resistant cells. We also confirmed by the increased protein levels of proapoptotic factors such as caspase 3, caspase 9, p53, and Bax after treatment with RGD–PAMAM–FP nanoaggregates and also downregulates antiapoptotic factors. Hence, FA–PTX co‐loaded, RGD‐functionalized PAMAM G4.5 dendrimers may be considered as an effective therapeutic strategy to induce apoptosis in P‐gp‐overexpressing, multidrug‐resistant cells. [ABSTRACT FROM AUTHOR]

In this study, the effect of caffeic acid ( CA) on both acute and chronic UVB-irradiation-induced inflammation and photocarcinogenesis was investigated in Swiss albino mice. Animals were exposed to 180 mJ cm−2 of UVB once daily for 10 consecutive days and thrice weekly for 30 weeks for acute and chronic study respectively. UVB exposure for 10 consecutive days showed edema formation, increased lipid peroxidation and decreased antioxidant status with activation of inflammatory molecules such as TNF- α, IL-6, COX-2 and NF- κ B. However, CA (15 mg per kg.b.wt.) administration before each UVB exposure decreased lipid peroxidation, inflammatory markers expression and enhanced antioxidant status probably through the activation of peroxisome proliferator-activated receptors ( PPAR γ) in the mice skin. PPAR γ is considered a potential target for photochemoprevention because it inhibits UVB-mediated inflammatory responses. In this study, UVB exposure for 30 weeks caused squamous cell carcinoma and upregulation of iNOS, VEGF and TGF- β and downregulation of p53 and tumor incidence in the mice skin. Both topical ( CAT) and intraperitoneal ( CAIP) treatment before each UVB exposure downregulates iNOS, VEGF, TGF- β, upregulates p53 and reduces tumors multiplicity in the mice skin. Thus, CA offers protection against UVB-induced photocarcinogenesis probably through activation of anti-inflammatory transcription factor PPAR γ in the mice. [ABSTRACT FROM AUTHOR]