Protective effects against and potential mechanisms underlying the effect of magnesium isoglycyrrhizinate in hypoxiareoxygenation injury in rat liver cells
Abstract
We examined the protective effects of magnesium isoglycyrrhizinate (MgIG) on hypoxia-reoxygenation injury in rat liver cells. Rat liver cells in the logarithmic growth phase were divided into the hypoxia-reoxygenation injury model group and MgIG pretreatment group (0.01, 0.1, 1, 10, 100 mg/mL). After 24-h pretreatment, we detected the effects of MgIG on liver cell viability using the methyl thiazolyl tetrazolium (MTT) assay at 6-h hypoxia and 4-h reoxygenation. After 24-h pretreatment, liver cells were randomly divided into the hypoxia-reoxygenation injury model group and low-, moderate-, and high-MgIG-concentration groups (0.1, 1, 10 mg/mL, respectively), and hypoxia and reoxygenation were simulated for 6 and 4 h, respectively. Cell morphology was observed by light microscopy. Nuclear factor-kB gene expression was analyzed by quantitative reverse transcription-polymerase chain reaction. MTT results showed that MgIG (0.1, 1, 10 mg/mL) improved the A-value of anoxia-reoxygenation injury in liver cells (P < 0.01) compared with that of the model group. Cells did not survive when the MgIG concentration was 100 mg/mL. At an MgIG concentration lower than 0.01 mg/mL, the A-value of the MTT group was higher than that of the model group (P > 0.05). Nuclear factor-kB mRNA expression (0.597 ± 0.062, 0.248 ± 0.067, 0.141 ± 0.029) in the low-, moderate-, and high-concentration groups was lower than that in the model group (P < 0.01). MgIG reduced hypoxia-reoxygenation injury of liver cells, indicating that it improved hepatic cell activity, inhibited lipid peroxidation and inflammatory reactions, and decreased nuclear factor-kB mRNA expression.
We examined the protective effects of magnesium isoglycyrrhizinate (MgIG) on hypoxia-reoxygenation injury in rat liver cells. Rat liver cells in the logarithmic growth phase were divided into the hypoxia-reoxygenation injury model group and MgIG pretreatment group (0.01, 0.1, 1, 10, 100 mg/mL). After 24-h pretreatment, we detected the effects of MgIG on liver cell viability using the methyl thiazolyl tetrazolium (MTT) assay at 6-h hypoxia and 4-h reoxygenation. After 24-h pretreatment, liver cells were randomly divided into the hypoxia-reoxygenation injury model group and low-, moderate-, and high-MgIG-concentration groups (0.1, 1, 10 mg/mL, respectively), and hypoxia and reoxygenation were simulated for 6 and 4 h, respectively. Cell morphology was observed by light microscopy. Nuclear factor-kB gene expression was analyzed by quantitative reverse transcription-polymerase chain reaction. MTT results showed that MgIG (0.1, 1, 10 mg/mL) improved the A-value of anoxia-reoxygenation injury in liver cells (P < 0.01) compared with that of the model group. Cells did not survive when the MgIG concentration was 100 mg/mL. At an MgIG concentration lower than 0.01 mg/mL, the A-value of the MTT group was higher than that of the model group (P > 0.05). Nuclear factor-kB mRNA expression (0.597 ± 0.062, 0.248 ± 0.067, 0.141 ± 0.029) in the low-, moderate-, and high-concentration groups was lower than that in the model group (P < 0.01). MgIG reduced hypoxia-reoxygenation injury of liver cells, indicating that it improved hepatic cell activity, inhibited lipid peroxidation and inflammatory reactions, and decreased nuclear factor-kB mRNA expression.