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目的探讨枸杞汁对邻苯二甲酸二乙基己基酯(DEHP)染毒所致氧化损伤和血脂异常的干预作用及差异。方法将实验大鼠分为对照组、DEHP组(1 500 mg/kg)、GSH干预组(500 mg/kg GSH+1 500 mg/kg DEHP)和枸杞汁干预组(枸杞原汁+1 500 mg/kg DEHP),连续灌胃7 d,测定大鼠血清及肝中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的活性以及血脂水平。结果与对照组相比,DEHP染毒会导致血清中GSH-Px活性、甘油三酯(TG)、高密度脂蛋白(HDL-C)浓度降低,差异有统计学意义(P<0.05或P<0.01),TG/HDL-C和非高密度脂蛋白胆固醇(non-HDL-C)浓度升高,差异有统计学意义(P<0.05或P<0.01),肝中GSH-Px、SOD活性差异有统计学意义(P<0.05或P<0.01);与DEHP组比较,枸杞汁和GSH均能使血清中GSH-Px活性升高,TG/HDL-C降低(P<0.05或P<0.01),枸杞汁组non-HDL-C、GSH组LDL-C浓度降低(P<0.05),2个干预组大鼠肝中SOD活性均低于DEHP组,上述差异均有统计学意义。结论 DEHP染毒会导致大鼠肝氧化损伤及血脂水平异常,枸杞汁与GSH的作用相似,即对DEHP诱导的氧化损伤和血脂异常具有良好的调节保护作用。
Objective To investigate the intervention effects and the differences of wolfberry juice on oxidative damage and dyslipidemia induced by diethylhexyl phthalate (DEHP). Methods The experimental rats were divided into control group, DEHP group (1 500 mg / kg), GSH intervention group (500 mg / kg GSH + 1 500 mg / kg DEHP) and Chinese wolfberry juice intervention group / kg DEHP) for 7 days. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and serum lipids in serum and liver of rats were measured. Results Compared with the control group, the concentration of GSH-Px, triglyceride (TG) and high density lipoprotein (HDL-C) in serum of DEHP group were significantly lower than those of the control group (P <0.05 or P < 0.01), TG / HDL-C and non-HDL-C, the difference was statistically significant (P <0.05 or P <0.01) (P <0.05 or P <0.01). Compared with DEHP group, the activity of GSH-Px in serum and the level of TG / HDL-C in serum of wolfberry juice and GSH decreased (P <0.05 or P <0.01) , LDL-C in non-HDL-C and GSH groups decreased (P <0.05) in the wolfberry juice group, while the SOD activity in the liver of the two intervention groups was lower than that in the DEHP group. These differences were statistically significant. Conclusion DEHP exposure can lead to liver oxidative damage and dyslipidemia in rats. The effect of wolfberry juice on GSH is similar, that is to say, DEHP has a good regulatory effect on the oxidative damage and dyslipidemia induced by DEHP.