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%的可溶性淀粉溶液，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P38 mRNA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、抑制羟自由基能力和POD活性，降低了Dex应激小鼠脾脏和胸腺MAPK信号通路中ASK1、JNK和P38 mRNA表达量以及脾脏ASK1、JNK和P38蛋白的表达量。BA对Dex造成的氧化损伤具有预防性的保护作用，并且这种保护作用与JNK-P38 MAPK信号通路相关。

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 P38 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 P38 in spleen and thymus of Dex group were significantly increased (P<0.01); compared with Dex group, the mRNA expressions of ASK1, JNK and P38 in spleen and thymus of 0.50 and 1.00 mg/kg BA groups were significantly decreased (P<0.05 or P<0.01). 3) Compared with NC group, the protein expressions of JNK and P38 in spleen of Dex group were significantly increased (P<0.01); compared with Dex group, the ASK1 protein expressions in spleen of 0.50 mg/kg BA group was significantly decreased (P<0.05), the protein expressions of JNK and P38 in spleen of 0.25, 0.50 and 1.00 mg/kg BA groups were significantly decreased (P<0.05 or P<0.01). In conclusion, BA pretreatment can increase T-AOC, ability of inhibiting hydroxyl radical and POD activity in liver, spleen and thymus of mice induced by Dex, decrease the gene expressions of ASK1, JNK and P38 in spleen and thymus and the protein expressions of ASK1, JNK and P38 in spleen of mice induced by Dex. BA shows preventive protection of oxidative damage induced by Dex, and the protection is related to JNK-P38 MAPK signal pathway.