Protective effects of Mangifera indica L. extract, mangiferin and selected antioxidants against TPA-induced biomolecules oxidation and peritoneal macrophage activation in mice

• Published in: Pharmacological research 2000-12, Vol.42 (6), p.565-573
• Main Authors: Sánchez, G.M., Re, L., Giuliani, A., Núñez-Sellés, A.J., Davison, G.P., León-Fernández, O.S.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; DNA Fragmentation - drug effects; Glutathione Peroxidase - blood; Lipid Peroxidation - drug effects; Macrophage Activation - drug effects; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - metabolism; Male; Mangifera indica, mangiferin, oxidative stress, vitamin C, vitamin E, β -carotene, free radicals; Mice; Oxidation-Reduction; Plants, Medicinal; Reactive Oxygen Species - metabolism; Superoxide Dismutase - blood; Tetradecanoylphorbol Acetate - pharmacology; Xanthenes - pharmacology; Xanthones
• ISSN: 1043-6618; 1096-1186
• DOI: 10.1006/phrs.2000.0727

We compared the protective abilities of Mangifera indica L. stem bark extract (Vimang® ) 50–250 mgkg−1, mangiferin 50 mgkg−1, vitamin C 100mgkg−1 , vitamin E 100 mgkg−1and β -carotene 50mgkg−1 against the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage in serum, liver, brain as well as in the hyper-production of reactive oxygen species (ROS) by peritoneal macrophages. The treatment of mice with Vimang ®, vitamin E and mangiferin reduced the TPA-induced production of ROS by the peritoneal macrophages by 70, 17 and 44%, respectively. Similarly, the H2O2levels were reduced by 55–73, 37 and 40%, respectively, when compared to the control group. The TPA-induced sulfhydryl group loss in liver homogenates was attenuated by all the tested antioxidants. Vimang ®, mangiferin, vitamin C plus E and β -carotene decreased TPA-induced DNA fragmentation by 46–52, 35, 42 and 17%, respectively, in hepatic tissues, and by 29–34, 22, 41 and 17%, in brain tissues. Similar results were observed in respect to lipid peroxidation in serum, in hepatic mitochondria and microsomes, and in brain homogenate supernatants. Vimang ® exhibited a dose-dependent inhibition of TPA-induced biomolecule oxidation and of H2O2production by peritoneal macrophages. Even if Vimang ®, as well as other antioxidants, provided significant protection against TPA-induced oxidative damage, the former lead to better protection when compared with the other antioxidants at the used doses. Furthermore, the results indicated that Vimang ® is bioavailable for some vital target organs, including liver and brain tissues, peritoneal exudate cells and serum. Therefore, we conclude that Vimang ® could be useful to prevent the production of ROS and the oxidative tissue damages in vivo.