Benzene (BZ) is an important occupational and environmental pollutant. Exposure to BZ may cause aplastic anemia which is characterized as bone marrow hematopoietic failure. In order to reduce the harmful effects of this pollutant, it is necessary to identify additional preventative measures. In this study, we investigated the protective effects of epimedium polysaccharide (EPS), a natural compound with antioxidant and immune-enhancing potency, on aplastic anemia induced by benzene exposure in mice. Male CD-1 mice were randomly divided into five groups including control, BZ (880 mg/kg), LE (EPS low-dose, 20 mg/kg + BZ), ME (EPS middle-dose, 100 mg/kg + BZ), and HE (EPS high-dose, 200 mg/kg + BZ) groups. Animals were exposed to BZ by subcutaneous injection in the presence or absence of EPS via oral administration. All mice were treated 3 times a week for 8 consecutive weeks to develop a mouse model of benzene-induced aplastic anemia (BIAA). Results showed that BZ induced a significant decrease in both white and red blood cells, platelet counts, and hemoglobin level compared with that in the control group (p<0.01). Treatment of EPS led to a protective effect against these changes particularly in the highest-dose group (HE, p<0.01). EPS also recovered the decreased number of nucleated cells in peripheral blood cell smears and femur biopsies by BZ exposure. The increased level of reactive oxygen species (ROS) in bone marrow mononuclear cells (BMMNCs) in mice from the BZ group was significantly lower (p<0.01) in the mice from the highest concentration of EPS (HE) group when compared with that from the control group. In addition, BZ exposure led to a significant increase in the apoptosis rate in BMMNCs which was prevented by EPS in a dose-dependent manner (p<0.01). The antiapoptosis effect of EPS was through reversing apoptotic proteins such as BAX, Caspase-9 and Caspase-3, and Bcl-2. Finally, EPS treatment partially restored the levels of T cells and the different subtypes except CD80+ and CD86+ compared with the BZ group (HE, p<0.05). These results suggest that EPS has protective effects against BIAA via antioxidative stress, immune modulation, and antiapoptosis mechanisms.
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机译：苯（BZ）是一个重要的职业和环境污染物。暴露于BZ可能导致具有增种性贫血，其特征为骨髓造血失效。为了减少这种污染物的有害影响，有必要确定额外的预防措施。在这项研究中，我们研究了淫羊藿多糖（EPS），天然化合物与抗氧化剂和免疫增强效力的保护作用，对小鼠苯暴露诱导的再生障碍性贫血。将雄性CD-1小鼠随机分为5组，包括对照，BZ（880mg / kg），LE（EPS低剂量，20mg / kg + BZ），ME（EPS中剂量，100 mg / kg + BZ ），他（EPS高剂量，200mg / kg + BZ）组。通过口服给药在皮疹存在或不存在EPS的情况下暴露于BZ。将所有小鼠每周治疗3次，连续8周，形成苯诱导的苯源性贫血（BIAA）的小鼠模型。结果表明，与对照组相比，BZ诱导白色和红细胞，血小板计数和血红蛋白水平的显着降低（P <0.01）。 EPS治疗导致对这些变化的保护作用，特别是在最高剂量组（HE，P <0.01）中。通过BZ暴露，EPS还回收了外周血细胞涂片和股骨活组织检查中的核细胞数量下降。与来自BZ组的小鼠中，从BZ组的小鼠中骨髓单核细胞（BMMNC）中的反应性氧物质（BMMNC）的增加水平显着降低（P <0.01），与此相比对照组。此外，BZ暴露导致BMMNC中凋亡率的显着增加，其通过EPS以剂量依赖性方式预防（P <0.01）。 EPS的抗痘病效应是通过逆转凋亡蛋白，例如Bax，Caspase-9和Caspase-3和Bcl-2。最后，EPS治疗部分恢复了除CD80 +和CD86 +以外的T细胞和不同亚型的水平，与BZ组（HE，P <0.05）相比。这些结果表明，EPS通过抗氧化应激，免疫调节和抗胃癌机制对BIAA具有保护作用。
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