Abstract
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.
Highlights
Benzene (BZ) is an organic solvent that is widely used as a precursor in the synthesis of numerous products such as rubbers, dyes, insecticides, and drugs [1]
A recent epidemiological study suggested that immune-mediated chronic inflammation response is involved in BZ-induced hematotoxicity [10]. e T-cell-mediated immune response is associated with exogenous antigens which leads to a response in hematopoietic cells and immune cells to the particular situation resulting in inflammation [11]
After 8 weeks of BZ and epimedium polysaccharide (EPS) treatment, a gradual increase in the body weights was recorded for the control group (25%), BZ group (11%), highest concentration of EPS (HE) group (17%), medium-dose EPS group (ME) group (13%), and low-dose EPS group (LE) group (13%) as compared with their initial body weights. e lowest body weight was observed in the BZ group (11%)
Summary
Benzene (BZ) is an organic solvent that is widely used as a precursor in the synthesis of numerous products such as rubbers, dyes, insecticides, and drugs [1]. E bone marrow is a site for the storage of blood cells and a key immune organ for adaptive and innate immune. A recent epidemiological study suggested that immune-mediated chronic inflammation response is involved in BZ-induced hematotoxicity [10]. BZ can cause bone marrow immunotoxicity partially through deregulating or suppressing T lymphocytes function [12] and cytokine production [13]. Clinical and animal experimental studies showed that BZ exposure resulted in an immune suppression accompanied by a significant decrease of CD3+ and CD4+ T lymphocytes [15, 16]. Ese studies suggested that impairment of T-cell-mediated immune function plays an important role in BZ-induced toxicity. Clinical and animal experimental studies showed that BZ exposure resulted in an immune suppression accompanied by a significant decrease of CD3+ and CD4+ T lymphocytes [15, 16]. ese studies suggested that impairment of T-cell-mediated immune function plays an important role in BZ-induced toxicity. erefore, immune modulation could be a potential target for protection against BZ-induced hematotoxicity [17]
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