Obesity-related neurodegenerative diseases are associated with elevated saturated fatty acids (SFAs) in the brain. An increase in SFAs, especially palmitic acid (PA), triggers neuron cell apoptosis, causing cognitive function to deteriorate. In the present study, we focused on the specific mechanism by which PA triggers SH-SY5Y neuron cell apoptosis. We found that PA induces significant neuron cell cycle arrest in the G₂/M phase in SH-SY5Y cells. Our data further showed that G₂/M arrest is involved in elevation of endoplasmic reticular (ER) stress according to an increase in p-eukaryotic translation inhibition factor 2α, an ER stress marker. Chronic exposure to PA also accelerates beta-amyloid accumulation, a pathological characteristic of Alzheimer’s disease. Interestingly, SFA-induced ER stress, G₂/M arrest and cell apoptosis were reversed by treatment with 2-bromopalmitate, a protein palmitoylation inhibitor. These findings suggest that protein palmitoylation plays a crucial role in SFA-induced neuron cell cycle G₂/M arrest, ER stress and apoptosis; this provides a novel strategy for preventing SFA-induced neuron cell dysfunction.

Aims: Methods: Results: Conclusions:

Thermal cooking changes the profile of phenolic compounds, but does not attenuate the anti-inflammatory activities of black rice

The objective of this study was to investigate the effects of Gelidium amansii, an edible red agar cultivated off the northeast coast of Taiwan, on the growth of two lines of cancer cells, murine hepatoma (Hepa-1) and human leukemia (HL-60) cells, as well as a normal cell line, murine embryo fibroblast cells (NIH-3T3). The potential role of G. amansii on the induction of apoptosis was also examined. The results indicated that all extracts from G. amansii, including phosphate-buffered saline (PBS) and methanol extracts from dried algae as well as the dimethyl sulfoxide (DMSO) extract from freeze-dried G. amansii agar, inhibited the growth of Hepa-1 and NIH-3T3 cells, but not the growth of HL-60 cells. Annexin V-positive cells were observed in methanol and DMSO extract-treated, but not PBS extract-treated Hepa-1 and NIH-3T3 cells, suggesting that the lipid-soluble extracts of G. amansii induced apoptosis. In summary, extracts of G. amansii from various preparations exhibited antiproliferative effects on Hepa-1 and NIH-3T3 cells, and apoptosis may play a role in the methanol and DMSO extract-induced inhibitory effects. However, the antiproliferative effects of PBS extracts was not through apoptosis. Moreover, the growth-inhibitory effects of G. amansii were not specific to cancer cells.

In this study, the effects of bioactive compounds derived from vegetables of the Brassica genus (Brassicaceae) including 2-phenylethyl isothiocyanate (PEITC), indole-3-carbinol (I3C), and indolo[3,2-b]carbazole (ICZ), on the inhibition of NO production in RAW 264.7 cells were explored. The results indicated that PEITC and I3C inhibited lipopolysaccharide (LPS)- and interferon-γ (IFN-γ)-induced NO production in RAW 264.7 cells, and this inhibition was in accordance with lowering the expression of iNOS protein and mRNA. On the contrary, ICZ, a derivative of I3C, had no significant effect on the stimulated NO production. In conclusion, the Brassica plants derivatives, PEITC and, to a lesser extent, I3C inhibit the LPS/IFN-γ-induced NO production by lowering iNOS protein and mRNA expression in RAW 264.7 cells, in which the PEITC had a more potent inhibitory effect. Nevertheless, ICZ exhibits no inhibitory effect on the activated NO production (Indole-3-carbinol = indole-3-methanol).

This study was aimed to examine the effects of indole-3-carbinol (I3C) andβ-phenylethyl isothiocyanate (PEITC), bioactive components present in cruciferous vegetable, on the production of inflammatory mediators, including nitric oxide (NO), tumor necrosis factor-α(TNF-α) and interleukin-10 (IL-10), in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophages. Possible mechanisms of the NO-inhibitory effects were also explored. The results indicated that I3C and PEITC inhibited NO production, and this suppression was associated with decreased production of TNF-αand IL-10 by activated macrophages. In addition, I3C suppressed NO production even after the inducible nitric oxide synthase (iNOS) protein had been produced, but such an inhibitory effect was not observed in cells treated with PEITC. Furthermore, both compounds reduced the NO contents generated from an NO donor in a cell-free condition, suggesting that the increased NO clearance may have contributed to the NO-inhibitory effects. In summary, both I3C and PEITC possessed antiinflammatory effects by inhibiting the productions of NO, TNF-α, and IL-10, although the NO-inhibitory effects may have involved in different mechanisms.