Purpose: To study the effect of the crude methanol extract of Garcinia kola seed on lipopolysaccharide (LPS)-induced tissue damage in rats
Objective: Costus afer is a perennial monocot consumed as a remedy for various ailments. The present study investigates the effect of C. afer stem extract on ferrous/ascorbate-induced lipid peroxidation in rat brain, liver, and kidney homogenates. The inherent antioxidant and free radical scavenging potentials of the extract were also assessed using various in vitro models. Methods: Homogenates of isolated tissues were prepared, and lipid peroxidation was induced using the ferrous/ascorbate system and subsequently incubated with various concentrations of the extract. The ability of the methanolic extract to scavenge hydroxyl radicals, hydrogen peroxide and its ability to reduce ferric ions were investigated. The total antioxidant potential through the phosphomolybdate method was also measured. Results: The results revealed that C. afer stem extract reduced tissue lipid peroxidation induced by ferrous/ascorbate. The extract also possessed significant antioxidant/ free radical scavenging activity through the other in vitro models. In all cases, the effects were concentration dependent. Conclusion: The methanolic extract of C. afer stem possessed significant antioxidant potential ascribable to important phytochemicals and could protect cells/tissues from reactive oxygen species-induced damage. Thus, the plant has high pharmacological and ethnobotanical prospects.
The effect of glycine and kolaviron on lipopolysaccharide-induced U937 cell damage and activation of U937-derived macrophages was studied. U937 cells were incubated with either glycine or kolaviron or both for 24 h before exposure to lipopolysaccharide. Cell viability and production of reactive oxygen species (ROS) were later assessed. In the other experiment, the U937 cells were transformed to the macrophage form using phorbol 12-myristate 13-acetate and incubated with or without glycine or kolaviron or both before exposure to lipopolysaccharide. Production of TNF-α, IL-1, IL-6 and NO were later assessed. The expression of the antioxidant enzymes- superoxide dismutase (SOD) and catalase (CAT) was also evaluated via reverse transcription polymerase chain reaction (RT PCR). It revealed that lipopolysaccharide caused significant cell death and production of reactive oxygen species that was reduced by glycine and kolaviron. Glycine and kolaviron also reduced lipopolysaccharide-mediated secretion of TNF-α, IL-1, IL-6 and NO in U937-derived macrophages. In some cases, pre-incubation of cells with both glycine and kolaviron was better than the individual responses. Glycine and kolaviron also reduced lipopolysaccharide-induced alterations in the expression of SOD and CAT (p<0.05). The study shows that both glycine and kolaviron (either separately or in combination) reduced lipopolysaccharide-mediated alterations in U937 cells and U937-derived macrophages.
The effects of selenium and glycine (either separately or in combination) on hydrogen peroxide-induced cell death on U937 cells and activation of U937-derived macrophages were investigated. In the first instance, U937 cells were incubated with or without selenium (Se) or glycine (GLY) or both (Se + GLY) for 24 h before exposure to hydrogen peroxide. Control cells were not incubated with Se, GLY or exposed to hydrogen peroxide. Cell viability was later assessed via trypan blue and MTT assays. For the other experiment, U937 cells were transformed to the macrophage form using phorbol 12-myristate 13-acetate before incubating with or without Se, GLY, Se + GLY. Contents were subsequently exposed to hydrogen peroxide and 24 h later assessed for the production of TNF-α, IL-1, IL-6 and the expression of iNOS and NF-κB. The results revealed that hydrogen peroxide caused significant cell death which was ameliorated by both Se and GLY. Pre-incubation of the cells with both Se and GLY did not significantly enhance cell numbers compared to GLY (p > 0.05). On the other hand, Se and GLY reduced hydrogen peroxide-mediated production of TNF-α, IL-1, IL-6 and expression of iNOS and NF-κB. Incubating the U937-derived macrophages with Se + GLY significantly ameliorated hydrogen peroxide-mediated activation of macrophages when compared to pre-treatments with Se or GLY (p < 0.05). The findings demonstrate that both Se and GLY reduced hydrogen peroxide-induced alterations in U937 cells and U937-derived macrophages. Implications of the findings are discussed.
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