沙棘油对镉致大鼠肝损伤的拮抗作用

Antagonistic Effects of Sea Buckthorn Oil on Hepatic Damage Induced by Cadmium in Rats

目的探讨沙棘油(SBO)对急性、亚慢性染镉致大鼠肝损伤的拮抗作用。方法急性实验时,对照组和染镉组均灌胃0.9%NaCl,SBO干预组灌胃5 ml/kg SBO(纯度为95%)。2 h后,对照组皮下注射0.9%NaCl,SBO干预组和染镉组皮下注射35μmol/kg CdCl2。亚慢性实验时,染镉组和SBO干预组皮下注射6μmol/kg CdCl2,对照组皮下注射0.9%NaCl,连续6周。然后SBO干预组灌胃5 ml/kg SBO,对照组和染镉组灌胃0.9%NaCl,共2周。腹主动脉取血并取肝脏,测定急性、亚慢性染镉大鼠血清乳酸脱氢酶(LDH)、谷丙转氨酶(GPT)活力,肝丙二醛(MDA)、谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)活力。结果急性、亚慢性镉染毒使大鼠血清LDH、GPT活力明显升高,肝MDA、GSH含量明显升高及SOD活力明显降低。SBO干预组可使急性染镉大鼠血清LDH、GPT活力,肝MDA、GSH含量分别降至单纯染镉组的71.5%(183.77,257.02)、58.3%(15.83,27.13)和74.8%(88.49,118.27)、64.9%(6.81,10.49),差异有统计学意义(P<0.01),肝SOD活力明显升高。亚慢性染镉时,SBO处理组血清GPT活力明显低于单纯染镉组,肝MDA、GSH含量明显下降,肝SOD活力明显升高,差异有显著性(P<0.01)。结论SBO对急性、亚慢性镉染毒致大鼠肝氧化损伤有一定的拮抗作用。

Objective To study the antagonistic effects of sea buckthorn oil （SBO） on acute and sub - chronic hepatotoxicity induced by cadmium. Methods In acute experimentation, the control and cadmium groups were both given intragastrically with 0.9% NaCl, the SBO group was pretreated intragastrically with SBO 5ml/kg . Two hours later, the control group was injected subcutaneously with 0.9% NaCl, the Cd group and SBO group were both given subcutaneously with cadmium chloride （CdCI2） 35μmol/kg . In sub - chronic experimentation, the control group was injected subcutaneously with 0.9 % NaCl, cadmium group and SBO pretreatmdnt group were both injected subcutaneously with CdCl2 6μmol/kg, for up to 6 weeks. Then the SBO pretreatment group was given SBO 5ml/kg by intragastric administration for 2 weeks. Control group and Cd group were given intragastrically with 0.9% NaCl at the same time. Liver and blood samples from the rats＇ abdominal aorta were collected. Activities of lactate dehydrogenase （LDH） and glutamate-pyruvate transaminase （GPT） in serum were determined. Levels of malonydialdehyde （MDA） and glutathione （GSH） and activity of superoxide dismutase （SOD） in the liver were measured. Results For the rats in acute and sub - chronic exposure to cadmium, serum activities of LDH and GPT increased significantly, levels of MDA and GSH increased significantly, activity of SOD declined sharply in the group exposed to Cd only. In acute experimentation, the activities of LDH and GPT sharply reduced in the SBO pretreatment group, the MDA and GSH contents in liver to 71.5 % （183.77, 257.02） and 58.3 % （15.83, 27.13）, 74.8 % （88.49, 118.27） and 64.9 % （6.81, 10.49） respectively compared with Cd exposure group （P 〈 0.01 ）. The activity of SOD in liver significantly increased. As compared with the rats treated with the subchronic exposure to Cd only, activity of GPT in serum, MDA and GSH contents in liver declined sharply, SOD increased significantly in the SBO group （P〈 0.01）. Conclusions Pretreatment with SBO in rats could antagonize acute and subchronic hepatotoxicity induced by cadmium to a certain extent.