Purification of Coffee Polyphenols Extracted from Coffee Pulps (Coffee arabica L.) Using Aqueous Two-Phase System.

Coffee pulp is an abundant residue from the coffee industry, but it still contains large amounts of valuable compounds such as polyphenols. The extraction of polyphenols from coffee pulp by the conventional method is accompanied by contaminated compounds. This study, therefore, applied an aqueous two-phase system consisting of different ratios of ethanol/ammonium sulfate to eliminate impurities from coffee-pulp crude extract. The purification efficiency was evaluated via total polyphenol content, antioxidant activity and two major polyphenols in coffee pulps including chlorogenic acid and caffeic acid. Results showed that phenolic compounds mostly predominated in the alcohol-rich phase in which the antioxidant activity was greatly increased after the purification process. Compared to un-purified crude-coffee extract, the antioxidant activity of the purified samples increased approximately 34%, which was assumed to occur due to the slight increase of chlorogenic acid and caffeic acid. Fourier-transform infrared spectroscopy supported the effectiveness of the purification process by eliminating some impurities.

Chlorogenic acid rich in coffee pulp extract suppresses inflammatory status by inhibiting the p38, MAPK, and NF-κB pathways.

Coffee pulp (CP) is a coffee byproduct that contains various active ingredients, namely, chlorogenic acid (CGA) and caffeine. These active compounds show several benefits, including antihyperlipidemia, antioxidants, and anti-inflammation. However, the anti-inflammatory properties of Coffea pulp extract (CPE) are unknown. This work determined the impact of CPE on lipopolysaccharide (LPS)-activated murine macrophage cells and the molecular mechanism behind this action. RAW 264.7 cells were exposed to varying doses of CPE with or without LPS. Inflammatory markers and their mechanism were studied. CPE therapy has been shown to suppress the synthesis of inflammatory cytokines and mediators, namely, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1ß, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nitric oxide (NO), as well as prostaglandin E2 (PGE2). Finally, CPE inactivated the nuclear factor-kappa B (NF-κB) and MAPK signaling pathways. Consequently, CPE might be used as a nutraceutical to treat inflammation and its related disorders.