重组人源性锰超氧化物歧化酶对小鼠紫外线辐射所致氧化应激的保护作用

Protective effect of rhMn-SOD against ultraviolet induced oxidative stress in mice

目的研究重组人源性锰超氧化物歧化酶(rhMn-SOD)对小鼠经A波紫外线(UV-A)辐射所致氧化应激损伤的保护作用。方法60只♂昆明种小鼠随机分为空白对照组、损伤模型组、天然铜锌超氧化物歧化酶(Cu,Zn-SOD)组及3个剂量rhMn-SOD给药组。每天于辐射前1 h给药,辐照时间4 h,连续9 d,d 10处死动物。检测肝、脑匀浆及红细胞(RBC)溶血液的丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)及总超氧化物歧化酶(SOD)。结果UV-A模型组的肝脑匀浆的3个抗氧化指标与空白对照组比较具差异有显著性意义(P<0.01),rhMn-SOD预防性给药组肝脏各指标与UV-A模型组相比差异均有显著性意义(P<0.05),并有剂量依赖性关系,但各组的红细胞指标差异均无显著性意义(P>0.05)。结论该UV-A辐射模型主要造成肝、脑氧化损伤,对红细胞无明显影响;rhMn-SOD对肝脏具有较好的保护作用。

AIM To study the effects of recombinant human manganese superoxide dismutase（rhMn-SOD） against oxidative stress in mice induced by ultraviolet-A（UV-A）. METHODS Sixty Kunming male mice were randomly divided into 6 groups： the control group and the model group, injected with 0.9% normal saline （NS）, and the native Cu,ZnSOD group and three doses of the rhMn-SOD trial groups, injected with relevant SOD, respectively. One hour after injection, all the mice were exposed to UV-A for 4 h during 9 d. In d 10 they were killed. The content of malondialdehyde （MDA）, the activities of glutathione peroxidase （GSH-Px） and total superoxide dismutase （SOD） in liver, brain and RBC were determined. RESULTS Three antioxidative parameters in the liver and brain of the model group were significantly different （P 〈 0.05）from those of the control group, proving the oxidative injury induced by UV-A on the mice＇s liver and brain. The oxidative injury induced by UV-A on the liver of experimental mice were obviously reversed by rhMn-SOD in a dose dependent manner（ P 〈 0.05）. But the difference in three parameters of RBC among 6 groups were no significant（ P 〉 0.05）. CONCLUSION The oxidative injury on the liver and brain of experimental mice can be induced by UV-A except RBC. The rhMn-SOD has an effective protection on the liver against this oxidative injury induced by UV-A.