DDC等药物对急性羰基镍中毒大鼠肝脏SOD活力及Cu-Zn SOD基因表达影响

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目的评价大鼠急性羰基镍中毒后多种药物及药物联合干预对于肝脏SOD活力及Cu-Zn SOD基因表达的影响。方法将SD大鼠分为正常对照组、染毒对照组和五个药物治疗组,药物治疗组大鼠静态吸入250mg/m3羰基镍染毒30min,分别于染毒后4h和30h腹腔注射二乙基二硫氨基甲酸钠(DDC)、甲泼尼龙、亚硒酸钠、DDC+甲泼尼龙、参附回阳汤,染毒对照组染毒后不予药物治疗,3d和7d时取材,应用黄嘌呤氧化酶测定法和反转录-聚合酶链式反应(RT-PCR)方法分别测定肝脏SOD活性并分析Cu-Zn SOD基因表达水平。结果与正常组相比较,染毒组肝脏SOD活力和Cu-Zn SOD基因表达均明显降低,差异有统计学意义(P<0.05)。染毒后4h给药,肝脏SOD活力明显高于染毒后30h给药,差异有统计学意义(P<0.05)。与染毒组相比较,染毒后4、30h给予DDC,3d和7d时肝脏SOD活力和CuZn SOD基因明显升高(P<0.05),30h时给予DDC,3d和7d时肝脏SOD活力明显升高(P<0.05);染毒后4h和30h给予甲泼尼龙,SOD和Cu-Zn SOD水平未见明显升高,差异无统计学意义(P>0.05);染毒后4h给予DDC+甲泼尼龙,SOD水平明显升高(P<0.05)。结论急性羰基镍中毒后,DDC对于逆转羰基镍急性中毒所造成的肝脏抗氧化物酶及其基因损伤效果确切,且早期给药效果优于晚期给药;DDC联合甲泼尼龙也可逆转肝脏抗氧化物酶的损伤,但对于基因层面的损伤应用意义不大;而亚硒酸钠和参附回阳汤对于逆转抗氧化物酶水平和基因损伤效果尚不确切。 Objective To evaluate the effects of multiple drugs and drugs on liver SOD activity and Cu-Zn SOD gene expression after acute carbonyl nickel poisoning in rats. Methods The SD rats were divided into normal control group, exposure control group and five drug treatment groups. The rats in the drug treatment group were inhaled 250mg / m3 nickel carbonyl for 30 minutes, respectively. The rats were injected intraperitoneally with diethyl Methyl dithiocarbamate (DDC), methylprednisolone, sodium selenite, DDC + methylprednisolone, Shenfu Huiyang decoction, the control group were not given drug treatment after exposure to toxic drugs, 3d and 7d when drawn, the application of xanthine The activities of SOD in the liver were measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) respectively. The expression of Cu-Zn SOD gene was analyzed. Results Compared with the normal group, the activity of SOD and the expression of Cu-Zn SOD in the liver of the treated group were significantly decreased, the difference was statistically significant (P <0.05). 4h after injection, SOD activity in liver was significantly higher than that after 30h administration, the difference was statistically significant (P <0.05). Compared with the control group, the activities of SOD and CuZn SOD in liver were significantly increased at 4 and 30 hours (P <0.05) and DDC at 30 and 30 days, respectively. The activities of SOD in liver increased significantly at 3d and 7d (P <0.05). Methylprednisolone was given at 4h and 30h after exposure. There was no significant difference in SOD and Cu-Zn SOD between the two groups (P> 0.05) Nylon, SOD levels were significantly increased (P <0.05). Conclusions After acute carbonyl nickel poisoning, DDC has the exact effect on reversing the hepatic antioxidant enzyme and its gene damage caused by acute nickel carbonyl poisoning, and the effect of DDC administration is better than that of late administration; DDC combined with methylprednisolone can also reverse the liver anti- Oxidase injury, but not for gene level damage application significance; and sodium selenite and Shenfu Huiyang Decoction for reversing the level of antioxidant enzymes and genetic damage effect is not clear.
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