Hsu Dur-Zong, Liu Ming-Yie
Graduate Institute of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.
Crit Care Med. 2004 Jan;32(1):227-31. doi: 10.1097/01.CCM.0000104947.16669.29.
The aim of this study was to determine the effects and the defense mechanisms of sesame oil on lipopolysaccharide-induced oxidative stress in rats.
Laboratory in vivo study of the effect of sesame oil on lipid peroxide, superoxide anion, superoxide dismutase, catalase, glutathione, and nitrite concentrations. To assess the effect of sesame oil on hepatic function, we determined serum aspartate aminotransferase, total bilirubin, and liver histology.
University laboratory.
Male SPF Wistar rats.
Blood testing, administration of oils, and liver biopsies.
Oxidative stress induced by lipopolysaccharide (5 mg/kg, intraperitoneally) was assessed by determination of lipid peroxidation. Sesame oil was given orally immediately after lipopolysaccharide administration, and lipid peroxidation concentrations were determined. The reactive oxygen species superoxide anion was measured by chemiluminescence analyzer. The enzyme activities of superoxide dismutase and catalase and the concentrations of glutathione and nitrite also were determined. Hepatic injury was evaluated by determining the concentrations of serum aspartate aminotransferase and total bilirubin and by liver histologic examination. Sesame oil significantly reduced lipid peroxidation but failed to affect nitrite concentrations in lipopolysaccharide-treated rats. Superoxide anion counts were decreased, and glutathione, but not superoxide dismutase or catalase, was increased in sesame oil-treated groups with lipopolysaccharide-induced oxidative stress. Only sesame oil-treated groups, but not corn oil- or mineral oil-treated groups, showed attenuated hepatic disorder induced by lipopolysaccharide. In addition, sesame oil given 6 hrs after lipopolysaccharide also attenuated lipid peroxidation and hepatic disorder. Furthermore, sesame oil given immediately or 6 hrs after lipopolysaccharide administration significantly reduced morphologic changes induced by lipopolysaccharide.
A single dose of sesame oil may attenuate oxidative stress and subsequently relieve hepatic disorder in endotoxemic rats.
本研究旨在确定芝麻油对脂多糖诱导的大鼠氧化应激的影响及其防御机制。
关于芝麻油对脂质过氧化物、超氧阴离子、超氧化物歧化酶、过氧化氢酶、谷胱甘肽和亚硝酸盐浓度影响的体内实验室研究。为评估芝麻油对肝功能的影响，我们测定了血清天冬氨酸转氨酶、总胆红素和肝脏组织学。
大学实验室。
雄性无特定病原体Wistar大鼠。
血液检测、油类给药和肝脏活检。
通过测定脂质过氧化来评估脂多糖（5毫克/千克，腹腔注射）诱导的氧化应激。脂多糖给药后立即口服芝麻油，并测定脂质过氧化浓度。通过化学发光分析仪测量活性氧超氧阴离子。还测定了超氧化物歧化酶和过氧化氢酶的酶活性以及谷胱甘肽和亚硝酸盐的浓度。通过测定血清天冬氨酸转氨酶和总胆红素浓度以及肝脏组织学检查来评估肝损伤。芝麻油显著降低了脂质过氧化，但对脂多糖处理的大鼠的亚硝酸盐浓度没有影响。在脂多糖诱导氧化应激的芝麻油处理组中，超氧阴离子计数减少，谷胱甘肽增加，但超氧化物歧化酶或过氧化氢酶没有增加。只有芝麻油处理组，而不是玉米油或矿物油处理组，显示出脂多糖诱导的肝脏疾病有所减轻。此外，脂多糖给药6小时后给予芝麻油也减轻了脂质过氧化和肝脏疾病。此外，脂多糖给药后立即或6小时给予芝麻油显著减少了脂多糖诱导的形态学变化。
单剂量芝麻油可能减轻内毒素血症大鼠的氧化应激并随后缓解肝脏疾病。
