| Summary: | 碩士 === 靜宜大學 === 食品營養研究所 === 98 === Hyperglycemia which major characterizes diabetes, may be related to inflammation and oxidative stress. Inflammation and oxidative stress were of the major risk factor for diabetic complications. The purpose of this study was to investigate the effect of high glucose or inflammation on the cell injury and oxidative stress of liver cell. Human hepatocellular carcinoma cell line (HepG2) was cultured with (5, 10, 15, 25, 35 mM) glucose and/or 0, 0.1, 1, 10, 20 ng/ml tumor necrosis factor-α (TNF-α) in the experiment. Cell viability, nitrite content, MDA content, for 24, 72, 120 hr after treatment and NF-κB protein expression were measured. Additional L-ascorbic acid or α-tocopherol (0, 1, 10,
50, 100 μM) was added to measure cell viability and nitrite content.
Results were HepG2 cell viability of groups treated with 25, 35 mM glucose and/or 20 ng/ml TNF-α exhibited significant lower than control group (5 mM glucose) in the same culture time. HepG2 cell viability of groups treated with 0.1, 1, 20 ng/ml TNF-α exhibited significant lower than 0 ng/ml TNF-α treated group for 24 hr. HepG2 cell viability of groups treated with 25 mM glucose and 20 ng/ml TNF-α exhibited significant higher than 25 mM glucose treated group for 120 hr. HepG2 cell NF-κB protein expression of groups treated with 35 mM glucose and/or 20ng/ml TNF-α exhibited significant higher than control group (5 mM glucose) for 24 hr, but nitrite content and MDA were not significantly different with each other, except that HepG2 cell nitrite content of groups treated with 10 ng/ml TNF-α exhibited significant lower than control group (0 ng/ml TNF-α) for 120 hr. HepG2 cell viability of groups treated with 100 μM L-ascorbic acid exhibited significant lower than control group (5 mM glucose) for 120 hr; HepG2 cell viability of groups treated with 1, 10 μM α-tocopherol exhibited significant lower than control group (5 mM glucose) for 24 hr; HepG2 cell nitrite product of groups treated with 50, 100 μM α-tocopherol exhibited significant higher than control group (5 mM glucose) for 72 hr. Generally, high glucose concentration induced cell injury, with mechanism was correlated to NF-κB protein
expression.
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