桦木酸对地塞米松致小鼠氧化应激的机制研究  

Mechanism of Betulinic Acid on Oxidative Stressed Mice Induced by Dexamethasone

作　　者：朱利娟[1,2] 易想炼 赵静 王喜红[1] POZNIAK Blazej[3] 文利新 邬静[1] 易金娥 ZHU Lijuan;YI Xianglian;ZHAO Jing;WANG Xihong;WEN Lixin;WU Jing;YI Jin’e(College of Veterinary Medicine,Hunan Agricultural University,Changsha 410128,China;Changsha Lvye Bio-Technology Co.,Ltd.,Changsha 410125 China;Department of Biochemistry,Pharmacology and Toxicology,Faculty of Veterinary Medicine,Wroc aw University of Environmental and Life Sciences,Wroclaw 50-375,Poland;Hunan Co-Innovation Center Production Safety,Changsha 410128,China)

机构地区：[1]湖南农业大学动物医学院,长沙410128 [2]长沙绿叶生物科技有限公司,长沙410125 [3]弗罗兹瓦夫环境与生命科学大学兽医学院,波兰弗罗兹瓦夫50-375 [4]湖南畜禽安全生产协同创新中心,长沙410128

出　　处：《动物营养学报》2018年第3期1035-1043,共9页CHINESE JOURNAL OF ANIMAL NUTRITION

基　　金：湖南省科技计划项目(2015NK3008)；湖南省教育厅项目(17A098)；湖南省自然科学基金项目(2015JJ2077)；国家级大学生创新创业训练计划项目[(G)SCX1609]

摘　　要：本试验旨在研究桦木酸(BA)对地塞米松(Dex)诱导氧化应激小鼠的保护作用和机制。将40只健康雄性昆明小鼠随机分为5组,即对照(NC)组、Dex组、0.25 mg/kg BA组、0.50 mg/kg BA组、1.00 mg/kg BA组。NC组和Dex组小鼠灌服1%的可溶性淀粉糊,其余各组按不同剂量的BA灌服,连续14 d后,除对照组注射生理盐水外,其余4组均腹腔注射Dex(25 mg/kg BW)诱导氧化应激模型。检测各组小鼠肝脏、脾脏和胸腺总抗氧化能力(T-AOC)、抑制羟自由基能力和过氧化物酶(POD)的活性,反转录(RT)-PCR检测脾脏和胸腺丝裂原活化蛋白激酶(MAPK)信号通路中凋亡信号调节激酶1(ASK1)、c-Jun氨基末端激酶(JNK)和P38基因的表达量,蛋白质免疫印迹(Western Blot)法检测脾脏MAPK信号通路中ASK1、JNK和P38蛋白的表达量。结果表明:1)与NC组相比,Dex组的肝脏T-AOC、抑制羟自由基能力,脾脏POD活性,胸腺T-AOC、抑制羟自由基能力均极显著下降(P<0.01);与Dex组相比,0.50和1.00 mg/kg BA组肝脏T-AOC、抑制羟自由基能力以及POD活性均显著或极显著的升高(P<0.05或P<0.01),0.50 mg/kg BA组脾脏T-AOC、0.50和1.00 mg/kg BA组脾脏抑制羟自由基能力、0.25和1.00 mg/kg BA组脾脏POD活性均显著或极显著的升高(P<0.05或P<0.01),0.50和1.00 mg/kg BA组胸腺T-AOC、抑制羟自由基能力和POD的活性均显著或极显著升高(P<0.05或P<0.01)。2)与NC组相比,Dex组脾脏和胸腺ASK1、JNK和P38 mRNA表达量均极显著升高(P<0.01);与Dex组相比,0.50和1.00 mg/kg BA组脾脏和胸腺ASK1、JNK和P38mRNA表达量均显著或极显著下降(P<0.05或P<0.01)。3)与NC组相比,Dex组脾脏JNK和P38蛋白的表达量极显著升高(P<0.01);与Dex组相比,0.50 mg/kg BA组脾脏ASK1蛋白的表达量显著降低(P<0.05),0.25、0.50和1.00 mg/kg BA组脾脏JNK和P38蛋白的表达量显著或极显著降低(P<0.05或P<0.01)。由此可见,BA预处理后,增强了Dex应激小鼠肝脏、脾脏和胸腺的T-AOC、抑制羟自由基能力The objective of this research was to evaluate the effects of betulinic acid(BA)on ameliorating dexamethasone(Dex)-induced oxidative damage and the mechanism for the BA-mediated antioxidative effects.Forty male healthy Kunming mice were randomly divided into 5 groups,which were control(NC)group,Dex group,0.25 mg/kg BA group,0.50 mg/kg BA group and 1.00 mg/kg BA group.NC and Dex groups were administered orally with 1%starch solution,and the other groups were administered orally with different doses of BA for 14 days.Except NC group,mice in the other groups were intraperitoneal injected Dex(25 mg/kg BW)to set up oxidative damage model.The total antioxidant capacity(T-AOC),ability of inhibiting hydroxyl radical and peroxidase(POD)activity in liver,spleen and thymus were determined.The gene expressions of apoptosis signal-regulating kinase 1(ASK1),c-Jun N-terminal kinase(JNK)and P 38 in spleen and thymus through mitogen-activated protein kinase(MAPK)signal transduction pathway were determined by RT-PCR.The protein expressions of ASK1,JNK and P38 in spleen through MAPK signal transduction pathway were determined by Western Blot.The results showed as follows:1)compared with NC group,the T-AOC,ability of inhibiting hydroxyl radical and POD activity in liver,and POD activity in spleen,and T-AOC and ability of inhibiting hydroxyl radical in thymus of Dex group were significantly decreased(P<0.01).Compared with Dex group,the T-AOC,ability of inhibiting hydroxyl radical and POD activity in liver of 0.50 and 1.00 mg/kg BA groups were significantly increased(P<0.05 or P<0.01);the T-AOC in spleen of 0.50 mg/kg BA group,the ability of inhibiting hydroxyl radical in spleen of 0.50 and 1.00 mg/kg BA groups,and the POD activity in spleen of 0.25 and 1.00 mg/kg BA groups were significantly increased(P<0.05 or P<0.01);the T-AOC,ability of inhibiting hydroxyl radical and POD activity in thymus of 0.50 and 1.00 mg/kg BA groups were significantly increased(P<0.05 or P<0.01).2)Compared with NC group,the mRNA expressions of ASK1,JNK and

关 键 词：桦木酸 地塞米松 氧化应激 丝裂原活化蛋白激酶 

分 类 号：S816.7[农业科学—饲料科学]