白藜芦醇对急性脊髓损伤早期脂质过氧化反应和活性氧水平的抑制作用

摘要/Abstract

摘要： 目的: 探讨脊髓损伤后使用白藜芦醇(resveratrol,Res) 对脊髓损伤(SCI) 早期脂质过氧化反应和活性氧水平的抑制作用。方法: 采用重物下落撞击法制备成年大鼠的SCI 模型, 于损伤后即刻腹腔注射给予Res 50, 100 mg·kg^-1 和甲基强的松龙(MPSS)100mg·kg^-1, 测定SCI 后1, 24, 48 h 时Res 组受损脊髓组织超氧化物歧化酶(SOD) 和脂质过氧化反应产物丙二醛(MDA) 及活性氧(ROS) 水平, 并与MPSS 组进行疗效对比。结果: Res 50mg·kg^-1与100 mg·kg^-1均能够显著提高SCI 后损伤部位SOD 水平和抑制MDA 产生(P<0.01), 以48 h 为最明显;显著降低ROS 水平(P<0.01), 也以48 h 最大, 抑制率大于40 %;且有明显剂量依赖性, 作用与MPSS 相当或更优。结论: Res 可以有效抑制脊髓损伤后早期受损局部脂质过氧化反应和活性氧水平, 对脊髓损伤有潜在的保护与治疗作用。

关键词: 白藜芦醇, 脊髓损伤, 超氧化物歧化酶, 丙二醛, 活性氧

Abstract: AIM: To study the effects of resveratral on lipid peroxidativereaction and reactive oxygen species (ROS) in experimental spinal cordinjury rats.METHODS: The weight-dropping method was used to produce the experimental spinal cordinjury (SCI) in adultrats. Resveratrol (Res) and methylprednisolone (MPSS) were given intraperitoneally by the bolus injections of 50, 100mg·kg^-1 and 100 mg·kg^-1, respectively, immediately after induction of SCI.And then the effects of Res were observed at 1, 24, 48 h after SCI compared with MPSS.RESULTS: Res could obvious prevented reduction of superoxide dismutase (SOD) activity and reduce malondialdehyde (MDA) production andinhibit the ROS level in the injured spinal cord tissue in comparison with the SCI model at the dose of 50 mg·kg^-1 and 100 mg·kg^-1, which the mostremarkable effects was at 48 h with the inhibition rate over 40 %.The effects of Res were the sameas or even greater than those of MPSS.CONCLUSION: Res may effectively protect the spinal cord from lipid peroxidativereaction and ROS damage in SCI.

Key words: resveratrol, spinal cordinjury(SCI), superoxide dismutase(SOD), malondialdehyde(MDA), reactive oxygen species(ROS)

中图分类号:

R962
R453.9

杨迎暴, 朴英杰. 白藜芦醇对急性脊髓损伤早期脂质过氧化反应和活性氧水平的抑制作用[J]. 中国临床药理学与治疗学, 2002, 7(3): 193-196.

CAO Cheng-Xi, HE You-Zhao, ZHOU Shu-Lin, QIAN Yi-Tai. Inhibition of resveratral on lipid peroxidativereaction and reactive oxygen species of early experimental rat spinal cordinjury[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2002, 7(3): 193-196.

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