Small phytochemicals have been successfully adopted as antibacterial chemotherapies and are being increasingly viewed as potential antibiofilm agents. Some of these molecules are known to repress biofilm and toxin production by certain bacterial and yeast pathogens, but information is lacking with regard to the genes allied with biofilm formation. The present study was performed to investigate the inhibitory effect of burdock root extract (BRE) and of chlorogenic acid (CGA; a component of BRE) on clinical isolates of . BRE and CGA exhibited significant antibiofilm activity against without inflicting any harm to its planktonic counterparts. In vitro assays supported the β-lactamase inhibitory effect of CGA and BRE while in silico docking showed that CGA bound strongly with the active sites of sulfhydryl-variable-1 β-lactamase. Furthermore, the mRNA transcript levels of two biofilm-associated genes (type 3 fimbriae and trehalose-6-phosphate hydrolase) were significantly downregulated in CGA- and BRE-treated samples. In addition, CGA inhibited biofilm formation by and without affecting their planktonic cell growth. These findings show that BRE and its component CGA have potential use in antibiofilm strategies against persistent infections.

Mannich bases and its derivatives are regarded as supreme pharmacophores in therapeutics. The study investigates the antimycotic potential of Mannich bases, 1-((1H-benzimidazol-1-yl) methyl) urea (C1) and 1-((3-hydroxynapthalen-2-yl) methyl) thiourea (C2), against Candida albicans. Biofilm and hyphal inhibitory activities of the Mannich bases were tested by crystal violet quantification, fluorescence imaging cAMP rescue, qRT PCR, and by molecular docking analysis. The compounds inhibited the biofilms of C. albicans and restrained the filamentation abilities of the pathogen. Structure-activity relationship studies revealed that the presence of urea or thiourea moiety in the tail section is essential for interacting with adenylate cyclase (AC). The Mannich bases seemed to block Ras-cAMP-PKA pathway by inhibiting second messenger activity required for hyphal induction and biofilm formation. In conclusion, the study warrants point-of-care testing of C1/C2 and provides a starting point for deriving several structurally modified Mannich bases which might plausibly replace the prevailing antimycotic drugs in future.

the present study evaluated the effect of Ficus benghalensis linn. (Moraceae) stem bark on porcine pancreatic α-amylase, rat intestinal α-glucosidase and sucrase. Further, the effect of heat treatment was also studied. Both untreated and heattreated samples inhibited α-amylase to a significant extent. Further, the aqueous extracts prepared form untreated and heat treated samples exhibited significant inhibition (p ≤ 0.05) of α-glucosidase and sucrase in a dose dependent manner. Heat treatment of the sample increased α-glucosidase and sucrase inhibitory activities at lower concentrations, however no statistical differences were observed at higher concentrations. Consequently, the untreated extracts showed IC 50 values of 158 and 193 μg mL-1 for α-glucosidase and sucrase respectively while, the heat-treated extracts showed the IC 50 values 77 and 141 μg mL-1 respectively. Further, a significant correlation (p ≤ 0.05; r = 0.698) was observed between α-glucosidase and sucrase inhibitory activities of both untreated and heat-treated extracts. The results clearly demonstrate that inhibition of carbohydrate hydrolyzing enzymes is one of the mechanism through which F. benghalensis bark exerts its hypoglycemic effect in vivo.

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