甘糖酯抗氧化作用的分子机制

目的探讨甘糖酯(PGMS)清除自由基抗氧化作用的分子机制。方法给大鼠ig高脂乳剂建立高脂血症模型,分成对照组、甘糖酯治疗组、甘糖酯+DDC组,治疗3周。检测血清、肝脏、脾脏和主动脉中丙二醛(MDA)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性,以及Cu,Zn-SOD mRNA的表达水平。结果甘糖酯治疗组大鼠,丙二醛(MDA)含量降低,SOD,GSH-Px和CAT的活性显著升高,Cu,Zn-SOD mRNA的表达水平增加;而甘糖酯和DDC联合用药治疗组,DDC抑制了甘糖酯诱导的Cu,Zn-SOD mRNA表达水平和SOD活性的升高,造成MDA含量的相应升高。结论甘糖酯通过诱导抗氧化酶SOD,GSH-Px和CAT的活性,增加Cu,Zn-SOD mRNA的表达水平,清除体内过多的氧自由基,达到抗氧化的目的。

Molecular mechanisms of antioxidant effects of propylene glycol mannate sulfate

AIM: To investigate the antioxidant mechanisms of propylene glycol mannate sulfate (PGMS) in hyperlipidemic rats. METHODS: Male Wistar rats were given high lipid emulsion diet to establish hyperlipidemic model. PGMS was given every day at different doses (37.8 and 75.6 mg.kg-1, ig) to hyperlipidemic rats for three weeks. In addition, diethyldithiocarbamate (DDC) was given 200 mg.kg-1.3 d-1 (i.p.) to inhibit SOD activity. Then, the MDA content was examined using TBA method to show the oxidation level, and the activities of SOD, GSH-Px and CAT were examined following the kit protocols to indicate the capability of eliminating OFR. RT-PCR was applied to study the expression of Cu, Zn-SOD mRNA in rat liver. RESULTS: The MDA content of PGMS treatment groups decreased markedly compared with hyperlipidemic group, and the activities of SOD, GSH-Px and CAT increased distinctly. Cu, Zn-SOD mRNA expression was significantly increased by PGMS treatment. Furthermore, the application of DDC(the SOD inhibitor) reduced total SOD activity and Cu, Zn-SOD mRNA expression induced by PGMS, and the content of MDA increased correspondingly. CONCLUSION: PGMS can induce the activities of antioxidant enzymes and the mRNA expression of Cu, Zn-SOD, which contribute to the elimination of oxygen free radical. This may explain the molecular mechanism of antioxidant effects of PGMS.