Synthesis and characterization of Sn‑doped TiO2 flm for antibacterial applications

Simple sol–gel method has been exploited to deposit Sn-doped TiO2 thin flms on glass substrates. The resultant coatings were characterized by X-ray difraction (XRD), UV–visible techniques (UV–Vis), Fourier transform infrared spectroscopy (FTIR), and photoluminescence analysis (PL). The XRD pattern reveals an increase in crystallite size of the prepared samples with the increasing doping concentration. A decrease in doping concentrating resulted in the decrease in bandgap values. The diferent chemical bonds on these flms were identifed from their FTIR spectra. The photoluminescence analysis shows an increase in the emission peak intensity with increasing dopant concentration, and this can be attributed to the efect created due to surface states. The prepared samples were tested as antibacterial agent toward both Gram-positive and Gram-negative bacteria like S.aureus (Staphylococcus aureus) and E.coli (Escherichia coli), respectively. The size of the inhibition zones indicates that the sample shows maximum inhibitory property toward E.coli when compared to S.aureus

Plant Isoquinoline Alkaloid Berberine Exhibits Chromatin Remodeling by Modulation of Histone Deacetylase To Induce Growth Arrest and Apoptosis in the A549 Cell Line

Histone deacetylases (HDACs) are a group of epigenetic enzymes that control gene expression through their repressive influence on histone deacetylation transcription. HDACs are probable therapeutic targets for cancer treatment, spurring the progress of different types of HDAC inhibitors. Further, natural-source-based derived bioactive compounds possess HDAC inhibitor property. In this way, we hypothesized that plant isoquinoline alkaloid berberine (BBR) could be a HDAC inhibitor in the human lung cancer A549 cell line. BBR represses total HDAC and also class I, II, and IV HDAC activity through hyperacetylation of histones. Furthermore, BBR triggers positive regulation of the sub-G₀/G₁ cell cycle progression phase in A549 cells. Moreover, BBR-induced A549 cell growth arrest and morphological changes were confirmed using different fluorescence-dye-based microscope techniques. Additionally, BBR downregulates oncogenes (TNF-α, COX-2, MMP-2, and MMP-9) and upregulates tumor suppressor genes (p21 and p53) mRNA and protein expressions. Besides, BBR actively regulates Bcl-2/Bax family proteins and also triggered the caspase cascade apoptotic pathway in A549 cells. Our finding suggests that BBR mediates epigenetic reprogramming by HDAC inhibition, which may be the key mechanism for its antineoplastic activity