机构地区:[1]Department of Cell Biology, University of Calabria, Rende, Italy [2]Department of Ecology, University of Calabria, Rende, Italy [3]Drogo Farm, Rocca Imperiale, Italy. [4]Research area MASDER sas, Marano Marchesato, Italy
出 处:《Food and Nutrition Sciences》2012年第12期1697-1702,共6页食品与营养科学(英文)
摘 要:The purpose of this study was to evaluate the ability of aqueous extract of Aloe barbadensis Miller (Aloe vera) on oxidative damage and Anion Exchanger 1 (AE1, also known as Band 3) expression in human erythrocytes exposed to the water soluble free radical initiator 2.2’-azobis-2-amidinopropano dihydrochloride (AAPH). In addition, total phenolic compounds in the extracts were determined as catechin equivalent and the various antioxidant activities were compared to natural and synthetic standard antioxidants such as BHA and ascorbic acid. Since Aloe vera extract did not cause a consumption of the cytosolic antioxidant, glutathione (GSH) when it was direct incubated with GSH in basic aerated aqueous solution, this indicates that Aloe vera extract does not proceed auto oxidation at this experimental condition. Furthermore, Aloe vera extract prevent the consumption of GSH, in radical treated RBCs. It also inhibit consumption of GSH when it was direct incubated with AAPH. Aloe vera gel extract inhibits the generation of diphenyl-2-picrylhy-drazyl (DPPH) and the scavenging activity was increased in a dose dependent manner. Aloe vera extract was shown the similar reducing power than standards BHT and ascorbic acid. Biochemical analysis by SDS-PAGE and western blotting showed that AAPH-induced oxidative stress increased the susceptibility of AE1 to proteolytic degradation. Of note, our data evidenced that Aloe vera treatment was able to partially restore the normal RBC membrane protein profiles in a dose-dependent manner. These results clearly demonstrate the antioxidative activity of Aloe vera gel extract that might be ascribed to a synergistic action of the bioactive compounds contained therein.The purpose of this study was to evaluate the ability of aqueous extract of Aloe barbadensis Miller (Aloe vera) on oxidative damage and Anion Exchanger 1 (AE1, also known as Band 3) expression in human erythrocytes exposed to the water soluble free radical initiator 2.2’-azobis-2-amidinopropano dihydrochloride (AAPH). In addition, total phenolic compounds in the extracts were determined as catechin equivalent and the various antioxidant activities were compared to natural and synthetic standard antioxidants such as BHA and ascorbic acid. Since Aloe vera extract did not cause a consumption of the cytosolic antioxidant, glutathione (GSH) when it was direct incubated with GSH in basic aerated aqueous solution, this indicates that Aloe vera extract does not proceed auto oxidation at this experimental condition. Furthermore, Aloe vera extract prevent the consumption of GSH, in radical treated RBCs. It also inhibit consumption of GSH when it was direct incubated with AAPH. Aloe vera gel extract inhibits the generation of diphenyl-2-picrylhy-drazyl (DPPH) and the scavenging activity was increased in a dose dependent manner. Aloe vera extract was shown the similar reducing power than standards BHT and ascorbic acid. Biochemical analysis by SDS-PAGE and western blotting showed that AAPH-induced oxidative stress increased the susceptibility of AE1 to proteolytic degradation. Of note, our data evidenced that Aloe vera treatment was able to partially restore the normal RBC membrane protein profiles in a dose-dependent manner. These results clearly demonstrate the antioxidative activity of Aloe vera gel extract that might be ascribed to a synergistic action of the bioactive compounds contained therein.
关 键 词:AE1 Transporter In Vitro OXIDATIVE Damage ALOE barbadensis MILLER Antioxidant Red Blood Cells Membrane Protein Free Radicals
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