Impact of roasting on javamide-I/-II in Arabica and Robusta coffee beans.

Javamide-I/-II are anti-inflammatory compounds found in coffee beans. However, potential effects of roasting on javamide-I/-II in coffee beans are currently unknown. Therefore, in this paper, the effects of roasting on javamide-I/-II were investigated in Arabica and Robusta beans. Coffee beans were roasted light, medium and dark, and the amounts of javamide-I/-II in the beans were quantified by a HPLC method. The data showed the different amounts of javamide-I/-II in the beans; not detected and ≤ 3.1 mg in Arabica beans, and 0.5-3.7 mg and 1.0-13.8 mg in Robusta beans, respectively. Furthermore, the data showed that roasting process significantly reduced the amounts of javamide-I/-II in both Arabica and Robusta beans (p < 0.05). These data were also confirmed by multivariate analyses. Additionally, these differences were validated in light, medium and dark roast coffee products in the market. Altogether, roasting can have a significant impact on javamide-I/-II amounts in coffee beans.

Javamide-II Inhibits IL-6 without Significant Impact on TNF-alpha and IL-1beta in Macrophage-Like Cells.

The main aim of this study is to find a therapeutic compound to inhibit IL-6, not TNF-alpha and IL-1beta, in macrophage-like cells, because the high-levels of IL-6 production by macrophages are reported to cause unfavorable outcomes under several disease conditions (e.g., autoimmune diseases, and acute viral infections, including COVID-19). In this study, the potential effects of javamide-II on IL-6, IL-1beta and TNF-alpha productions were determined using their ELISA kits in macrophage-like THP-1 cells. Western blots were also performed using the same cells, to determine its effects on signaling pathways (ERK, p38, JNK, c-Fos, ATF-2, c-Jun and NF-κB p65). At concentrations of 0.2-40 µM, javamide-II inhibited IL-6 production significantly in the THP-1 cells (IC50 of 0.8 µM) (P < 0.02). However, javamide-II did not inhibit IL-1beta or TNF-alpha productions much at the same concentrations. In addition, the treatment of javamide-II decreased the phosphorylation of p38 without significant effects on ERK and JNK phosphorylations in the THP-1 cells. Furthermore, the p38 inhibition, followed by the reduction of ATF-2 phosphorylation (not c-Fos, c-Jun or NF-κB p65), led to the suppression of IL-6 mRNA expression in the cells (P < 0.02). The data indicate that javamide-II may be a potent compound to inhibit IL-6 production via suppressing the p38 signal pathway, without significant effects on the productions of TNF-alpha and IL-1beta in macrophage-like THP-1 cells.