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目的研究氯化铝(AlCl3)染毒对大鼠的心脏毒性及铝螯合剂1,2-二甲基-3-羟基-4-吡啶酮(DFP)的保护作用。方法35只雄性Wistar大鼠,按体质量随机分为阴性对照组、铝染毒组及DFP低、中、高剂量组。AlCl3172.5mg/(kg.d)染毒8周后分别给予不同剂量的DFP2周,测定血清中乳酸脱氢酶(LDH)、肌酸激酶(CK)、谷草转氨酶(AST)的活力,心肌组织中超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力及脂质过氧化产物丙二醛(MDA)的含量,心肌组织中铝、锌、铜、铁、钙、镁的含量。结果铝染毒组大鼠血清LDH、CK的活力及心肌中MDA的含量均明显高于阴性对照组(P<0.01),心肌铁含量及GSH-Px的活力低于阴性对照组(P<0.05,P<0.01);DFP低、中、高剂量组中LDH、GSH-Px的活力低于铝染毒组(P<0.01),高剂量组CK的活力低于铝染毒组(P<0.05);且高剂量组各项指标与阴性对照组相比差异无统计学意义(P>0.05);血清AST的活力及心肌铜、锌、钙、镁的含量在各组间比较差异无统计学意义(P>0.05)。结论AlCl3可致大鼠心肌损伤,铝螯合剂DFP在排铝的同时,不影响心肌中必需元素的含量,改善AlCl3所致的心肌损伤。
Aim To study the cardiotoxicity of aluminum chloride (AlCl3) in rats and the protective effect of aluminum chelator 1,2-dimethyl-3-hydroxy-4-pyridone (DFP). Methods Thirty-five male Wistar rats were randomly divided into negative control group, aluminum exposure group and DFP low, medium and high dose groups. AlCl3172.5mg / (kg.d) for 8 weeks were given different doses of DFP for 2 weeks, serum lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST) activity, myocardial tissue The activities of SOD, GSH-Px and malondialdehyde (MDA) in myocardial tissue were measured. The contents of Al, Zn, Cu, Iron, calcium, magnesium content. Results The levels of serum LDH and CK and the content of MDA in myocardium were significantly higher in the aluminum-exposed group than those in the negative control group (P <0.01). The content of iron in the heart and the activity of GSH-Px were lower than those in the negative control group , P <0.01). The activities of LDH and GSH-Px in low, middle and high dose DFP groups were lower than those in aluminum group (P <0.01) ), And there was no significant difference between the high-dose group and the negative control group (P> 0.05). The serum AST and the content of copper, zinc, calcium and magnesium in the myocardium were not significantly different between the groups Significance (P> 0.05). Conclusion AlCl3 can induce myocardial injury in rats. Aluminum-chelating agent DFP does not affect the content of essential elements in myocardium and improves the myocardial injury induced by AlCl3.