桦木酸对Dex致小鼠氧化损伤的保护作用

Protective effect of betulinic acid on oxidative damage induced by dexamethasone in mice

为了研究桦木酸(betulinic acid,BA)对地塞米松(dexamethasone,Dex)致氧化损伤的保护作用。将35只健康雄性KM小鼠随机分为5组,即对照组、Dex组、BA低、中、高剂量(0.25、0.5、1 mg/kg)+Dex组。对照组和Dex组灌服1%的可溶性淀粉,其余各组灌服混悬于可溶性淀粉中不同剂量的BA,1次/d,连续14d后,除对照组注射生理盐水外,其余4组均腹腔注射地塞米松(25 mg/kg)诱导氧化应激模型。15h后,处死小鼠,收集淋巴器官和肝脏。检测小鼠淋巴细胞的活性以及活性氧(ROS)水平,肝脏、脾脏和胸腺的超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性以及丙二醛(MDA)含量。结果显示,BA预处理后,能显著降低Dex诱导氧化损伤小鼠ROS水平和MDA含量,提高脾淋巴细胞和胸腺淋巴细胞的活性,增强小鼠SOD和GSH-Px活性,且呈量效关系。表明BA能加速细胞清除活性氧自由基,增强小鼠抵抗氧化损伤的能力,对Dex诱导的氧化损伤有一定的保护作用。

To explore the protective effect of betulinic acid （BA） on oxidative damage induced by dexamethasone （Dex）. A total of 35 male Kunming mice were randomly divided into 5 groups, the control group,the Dex group ,the low, midium and high-dosage of BA with Dex group. The control group was administered orally with 1 starch and the other groups were administered orally with different doses of BA （0.25,0.5 ,and 1.0 mg/kg） daily for 14 d. The model of oxidative damage was set up in mice induced by Dex at the dosage of 25 mg/kg bw after last administration of BA. Fifteen hours later, cell viability and reactive oxygen species （ROS）level of lymphocytes, the activities of superoxide dismutase （SOD） and glutathione perioxidase （GSH-Px）, the content of malondialdehyde （MDA） in liver,thymus and spleen were measured. The results showed that BA pretreatment enhanced significantly cell viability and reduced ROS levels of lymphocytes in mice induced by Dex in a dose dependent manner. The activities of SOD, GSH-Px were increased remarkably,while the MDA content of liver,spleen and thymus were decreased by BA pretreatment after Dex-indueed oxidative damage in a dosedependent manner. The results suggested that BA effectively attenuated the damage of Dexinduced oxidative.