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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Cytoprotective effect of the fruits of Lycium chinense Miller against oxidative stress-induced hepatotoxicity.
Journal of Ethnopharmacology 2010 July 21
AIM OF THE STUDY: Fruits of Lycium chinense Miller (Solanaceae), distributed in northeast Asia, have gained attraction for their hepatoprotective role in traditional oriental medicine. The excessive production of reactive oxygen species (ROS) is hazardous for living organisms and damage major cellular constituents such as DNA, lipid, and protein. The cytoprotective effect of Lycium chinense fruits (Lycium extract) was assessed against H(2)O(2)-induced Chang liver cell damage.
MATERIALS AND METHODS: The effect of Lycium extract against H(2)O(2)-induced cell death was determined by the MTT assay. Radical scavenging activity was determined through the assessments of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, intracellular ROS, hydroxyl radicals, and superoxide. The inductions of antioxidant enzymes were determined via their protein expressions and activities. DNA damage was measured using comet assay and expression of phospho-histone H2A.X. Lipid peroxidation was measured using 8-isoprostane level and fluorescent probe. Protein modification was measured using protein carbonyl moiety.
RESULTS AND CONCLUSION: Lycium extract scavenged the DPPH free radicals, intracellular ROS, hydroxyl radicals, and superoxide. Lycium extract recovered activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased by H(2)O(2). Lycium extract decreased DNA damage, lipid peroxidation and protein carbonyl values increased by H(2)O(2) exposure. In addition, Lycium extract increased the cell viability of Chang liver cells exposed to H(2)O(2) via inhibition of apoptosis. These results show that Lycium extract protected Chang liver cells against oxidative stressed cell damage by H(2)O(2) via scavenging ROS and enhancing antioxidant enzyme activity.
MATERIALS AND METHODS: The effect of Lycium extract against H(2)O(2)-induced cell death was determined by the MTT assay. Radical scavenging activity was determined through the assessments of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, intracellular ROS, hydroxyl radicals, and superoxide. The inductions of antioxidant enzymes were determined via their protein expressions and activities. DNA damage was measured using comet assay and expression of phospho-histone H2A.X. Lipid peroxidation was measured using 8-isoprostane level and fluorescent probe. Protein modification was measured using protein carbonyl moiety.
RESULTS AND CONCLUSION: Lycium extract scavenged the DPPH free radicals, intracellular ROS, hydroxyl radicals, and superoxide. Lycium extract recovered activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased by H(2)O(2). Lycium extract decreased DNA damage, lipid peroxidation and protein carbonyl values increased by H(2)O(2) exposure. In addition, Lycium extract increased the cell viability of Chang liver cells exposed to H(2)O(2) via inhibition of apoptosis. These results show that Lycium extract protected Chang liver cells against oxidative stressed cell damage by H(2)O(2) via scavenging ROS and enhancing antioxidant enzyme activity.
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