RESUMO
Mass production of microalgae is a research focus owing to their promising aspects for sustainable food, biofunctional compounds, nutraceuticals, and biofuel feedstock. This study uses a novel approach to enhance microalgae-derived biomass and metabolites by using an aggregation-induced emission (AIE) photosensitizer (PS), CN-TPAQ-PF6 ([C32H23N4]+). The unique AIE features of CN-TPAQ-PF6 facilitate nano-aggregation in aquatic media for an effective light spectral shift for photosynthetic augmentation in a green microalga, Chlamydomonas reinhardtii. The high reactive oxygen species (ROS) production capacity and redox-based cellular modulations reveal its potential to upsurge algal growth and lipid biosynthesis and fabricate fatty acid profiles in the metabolic pathways. Algal cells are labeled with other AIE-based nanoprobes, which are suitable as an in vivo visualization toolkit with superior fluorescence. Furthermore, cytotoxicity analysis of CN-TPAQ-PF6 on the HaCat cell line confirms that this AIE PS is biocompatible without adverse impact on living cells. The results demonstrate the property of AIE PS for the first time in enhancing algal growth and lipid accumulation simultaneously.
RESUMO
Crinum asiaticum L. (Amaryllidaceae) is a perennial bulbous herb, locally utilized for possessing multifaceted pharmacological properties including anticancer, immune-stimulating, analgesic, antiviral, antimalarial, antibacterial and antifungal, in addition to its popularity as an aesthetic plant. Separation of MeOH extract of C. asiaticum leaves yielded three known compounds as cycloneolitsol (1), hippeastrine (2) and ß-sitosterol (3). Among these, compounds 1 and 2 were subjected to the cytotoxic assay and found that they induced mild effect against HCT116, Huh7 and DU145 cell lines with the IC50 values from 73.76 to 132.53 µM. When tested for TRAIL-resistance abrogating activity, 1 (100 µM) along with TRAIL (100 ng/mL) showed moderate activity in AGS cells producing 25 % more inhibition than the agent alone. Whereas 2 (20 and 30 µM) in combination with TRAIL (100 ng/mL) exhibited strong activity in abrogating TRAIL-resistance and caused 34 % and 36 % more inhibition in AGS cells, respectively. The in-silico studies of compound 2 revealed high docking hits with the TRAIL-associated anti-apoptotic proteins which give a justification for the regulatory interactions to induce such abrogating activity. It is still recommended to conduct further investigations to understand their exact molecular mechanism.