T-2 toxin, which is mainly produced by specific strains of Fusarium in nature, can induce immunotoxicity and oxidative stress, resulting in immune organ dysfunction and apoptosis. Betulinic acid (BA), a pentacyclic triterpenoids from nature plants, has been demonstrated to possess immunomodulating and antioxidative bioactivities. The purpose of the study was to explore the effect of BA on T-2 toxin-challenged spleen oxidative damage and further elucidate the underlying mechanism. We found that BA not only ameliorated the contents of serum total cholesterol (TC) and triglyceride (TG) but also restored the number of lymphocytes in T-2 toxin-induced mice. BA dose-dependently reduced the accumulation of reactive oxygen species (ROS), enhanced superoxide dismutase (SOD) activity, and decreased malondialdehyde (MDA) content, as well as increased the total antioxidant capacity (T-AOC) in the spleen of T-2-toxin-exposed mice. Moreover, BA reduced inflammatory cell infiltration in the spleen, improved the morphology of mitochondria and enriched the number of organelles in splenocytes, and dramatically attenuated T-2 toxin-triggered splenocyte apoptosis. Furthermore, administration of BA alleviated the protein phosphorylation of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinases (ERK); decreased the protein expression of kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein1 (Keap1); and increased the protein expression of nuclear factor erythroid 2 [NF-E2]-related factor (Nrf2) and heme oxygenase-1 (HO-1) in the spleen. These findings demonstrate that BA defends against spleen oxidative damage associated with T-2 toxin injection by decreasing ROS accumulation and activating the Nrf2 signaling pathway, as well as inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway.

中文翻译：

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桦木酸通过激活Nrf2和抑制MAPK信号通路减轻急性腹膜接触T-2毒素引起的脾氧化损伤。

T-2毒素，主要由镰刀菌的特定菌株产生在自然界中，可诱发免疫毒性和氧化应激，导致免疫器官功能障碍和细胞凋亡。桦木酸（BA）是来自自然植物的五环三萜类化合物，已被证明具有免疫调节和抗氧化的生物活性。该研究的目的是探讨BA对T-2毒素挑战的脾脏氧化损伤的作用，并进一步阐明其潜在机制。我们发现BA不仅改善了血清总胆固醇（TC）和甘油三酸酯（TG）的含量，而且还恢复了T-2毒素诱导的小鼠的淋巴细胞数量。BA剂量依赖性地减少了活性氧（ROS）的积累，增强了超氧化物歧化酶（SOD）活性并降低了丙二醛（MDA）含量，以及增加了暴露于T-2-毒素的小鼠脾脏中的总抗氧化能力（T-AOC）。此外，BA减少了脾脏中炎性细胞的浸润，改善了线粒体的形态，丰富了脾细胞中的细胞器数量，并显着减弱了T-2毒素触发的脾细胞凋亡。此外，BA的施用减轻了p38，c-Jun N末端激酶（JNK）和细胞外信号调节激酶（ERK）的蛋白质磷酸化。降低与CNC同源性[ECH]相关的蛋白1（Keap1）的海藻样类红细胞衍生蛋白的蛋白表达；并增加脾脏中核因子红系2 [NF-E2]-相关因子（Nrf2）和血红素加氧酶-1（HO-1）的蛋白表达。