Simultaneous enhancement of lipid biosynthesis and solvent extraction of Chlorella using aminoclay nanoparticles.

Magnesium aminoclay nanoparticles (MgANs) exert opposing effects on photosynthetic microalgae by promoting carbon dioxide (CO2) uptake and inducing oxidative stress. This study explored the potential application of MgAN in the production of algal lipids under high CO2 concentrations. The impact of MgAN (0.05-1.0 g/L) on cell growth, lipid accumulation, and solvent extractability varied among three tested oleaginous Chlorella strains (N113, KR-1, and M082). Among them, only KR-1 exhibited significant improvement in both total lipid content (379.4 mg/g cell) and hexane lipid extraction efficiency (54.5%) in the presence of MgAN compared to those of controls (320.3 mg/g cell and 46.1%, respectively). This improvement was attributed to the increased biosynthesis of triacylglycerols and a thinner cell wall based on thin-layer chromatography and electronic microscopy, respectively. These findings suggest that using MgAN with robust algal strains can enhance the efficiency of cost-intensive extraction processes while simultaneously increasing the algal lipid content.

Enhancement of astaxanthin production by Haematococcus pluvialis using magnesium aminoclay nanoparticles.

Improving the content and production of high-value ketocarotenoid pigments is critical for the commercialization of microalgal biorefineries. This study reported the use of magnesium aminoclay (MgAC) nanoparticles for enhancement of astaxanthin production by Haematococcus pluvialis in photoautotrophic cultures. Addition of 1.0 g/L MgAC significantly promoted cellular astaxanthin biosynthesis (302 ± 69 pg/cell), presumably by inducing tolerable oxidative stress, corresponding to a 13.7-fold higher production compared to that in the MgAC-untreated control (22 ± 2 pg/cell). The lipid content and cell size of H. pluvialis improved by 13.6- and 2.1-fold, respectively, compared to that of the control. Despite reduced cell numbers, the overall astaxanthin production (10.3 ± 0.4 mg/L) improved by 40% compared to the control (7.3 ± 0.6 mg/L), owing to improved biomass production. However, an MgAC dosage above 1.0 g/L inhibited biomass production by inducing electrostatic cell wall destabilization and aggregation. Therefore, MgAC-induced stimulation of algae varies widely based on their morphological and physiological characteristics.

S-allyl cysteine alleviates nonsteroidal anti-inflammatory drug-induced gastric mucosal damages by increasing cyclooxygenase-2 inhibition, heme oxygenase-1 induction, and histone deacetylation inhibition.

BACKGROUND AND AIM: Nonsteroidal anti-inflammatory drugs (NSAIDs), the most highly prescribed drugs in the world for the treatment of pain, inflammation, and fever, are associated with gastric mucosal damages including ulcer directly or indirectly. This study was aimed to document the preventive effects of an organosulfur constituent of garlic, S-allyl cysteine (SAC), against NSAIDs-induced gastric damages, as well the elucidation of its pharmacological actions, such as anti-inflammatory, anti-oxidative, and cytoprotective actions. METHODS: Different doses of SAC were administrated intragastrically before the indomethacin administration. After killing, in addition to gross and pathological evaluations of ulcer, the expressions of inflammatory mediators, including cyclooxygenase-2, prostaglandin E2 , IL-1ß, tumor necrosis factor-α, IL-6, and anti-oxidant capacity, were analyzed by Western blot analysis or ELISA, respectively. Transferase deoxytidyl uridine end labeling assay, periodic acid and Schiff staining, F4/80 staining, and CD31 staining were compared among doses of SAC. Detailed documentation of in vitro biological actions of SAC, including NF-κB, histone deacetylator inhibition, phase 2 enzyme, and MAPKs, was performed. RESULTS: SAC was very effective in preventing indomethacin-induced gastric damages in a low dose through significant decreases in macrophage infiltration as well as restorative action. Indomethacin-induced expressions of inflammatory mediators were all significantly attenuated with SAC in accordance with histone deacetylator inhibition. In addition, SAC significantly increased the total anti-oxidant concentration and mucus secretion, and allows for a significant induction of HO-1. However, these preventive effects of SAC were dependent on dosage of SAC; higher dose above 10 µM paradoxically aggravated NSAID-induced inflammation. CONCLUSION: Synthetic SAC can be promising therapeutics agent to provide potent anti-inflammatory, anti-oxidative, and mucosa protective effects against NSAID-induced damages.