Grewia tiliaefolia and its active compound vitexin regulate the expression of glutamate transporters and protect Neuro-2a cells from glutamate toxicity.

AIM: Glutamate is a major neurotransmitter involved in several brain functions and glutamate excitotoxicity is involved in Alzheimer's disease (AD). In the current study, the neuroprotective effect of the Indian medicinal plant Grewia tiliaefolia (GT) and its active component vitexin was evaluated in Neuro-2a cells against glutamate toxicity. MATERIALS AND METHODS: Neuro-2a cells were exposed to glutamate to cause excitotoxicity and the neuroprotective effect of GT and vitexin were evaluated using biochemical studies (estimation of reactive oxygen species, reactive nitrogen species, protein carbonyl content, lipid peroxidation level, mitochondrial membrane potential and caspase-3 activity), molecular docking studies, gene expression and western blot analysis. KEY FINDINGS: Glutamate exposure to Neuro-2a cells induced oxidative stress, loss of membrane potential, suppressed the expression of antioxidant response genes (Nrf-2, HO-1, NQO-1), glutamate transporters (GLAST-1, GLT-1) and induced the expression of NMDAR, Calpain. However, pre-treatment of cells with GT/vitexin inhibited oxidative stress mediated damage by augmenting the expression of Nrf-2/HO-1 pathway, inducing the expression of glutamate transporters and downregulating Calpain, NMDAR. Molecular docking showed that vitexin effectively binds to NMDAR and GSK-3ß and thereby can inhibit their activation. GT/vitexin also inhibited glutamate induced Bax expression. SIGNIFICANCE: Methanol extract of G. tiliaefolia and its active component vitexin can act in an antioxidant dependent mechanism as well as by regulating glutamate transporters in mitigating the toxicity exerted by glutamate in Neuro-2a cells. Our results conclude that GT/vitexin can act as potential drug leads for the therapeutic intervention of AD.

Inhibitory Effect of Biosynthesized Silver Nanoparticles from Extract of Nitzschia palea Against Curli-Mediated Biofilm of Escherichia coli.

Extended spectrum beta lactamase (ESBL) are emerging beta-lactamases in Gram-negative pathogens, causing serious problems in hospitalized patients worldwide. Biofilm mode of virulence has decreased the efficiency of antibiotics used for treatment against ESBL pathogens. Therefore, there is an urgent need for alternative agents such as nanoparticles that can prevent and inhibit the biofilm formation. The aim of the present study was to inhibit the biofilm formed by ESBL-producing Escherichia coli using silver nanoparticles (AgNPs) synthesized with fresh water diatom (Nitzschia palea). AgNPs were characterized using UV-Vis spectroscopy, Fourier transform infrared (FTIR) spectroscopy, field emission scanning electron microscope (FESEM), energy-dispersive X-ray spectroscopy (EDX), and XRD. AgNPs at their biofilm inhibitory concentration (BIC) of 300 ng ml-1 significantly reduced the biofilm formed by E. coli. Interestingly, Congo red assay revealed the reduction of curli, essential for biofilm formation in the presence of AgNPs. Light and CLSM examination of the biofilm images also validated that in the presence of AgNPs, the biofilm architecture was disintegrated and the thickness was significantly reduced. Overall, the present study exemplifies the use of AgNPs as a plausible alternative for conventional coating agents on implant devices to prevent and control biofilm-associated urinary tract infections.