二-(2-乙基己基)邻苯二甲酸(DEHP)污染环境,对人类和动物健康构成重大风险。因此,需要研究针对DEHP诱导的肝毒性的成功预防策略.沙林水合物(MH),黄烷醇化合物,对各种环境污染物具有有毒的预防属性。然而,尚未研究MH对DEHP诱导的肝毒性的影响。雌性瑞士白化病小鼠分为四组:对照组,DEHP(口服500mg/kg,DEHP加MH10mg/kg,和DEHP加MH100mg/kg,持续14天。结果表明,MH治疗通过降低丙氨酸转氨酶(ALT)改善DEHP诱导的肝功能障碍,天冬氨酸转氨酶(AST),总胆红素,肝脏组织结构,纤维化,和氧化应激的标志物。此外,DEHP增加细胞凋亡,活性半胱天冬酶3增加,B细胞淋巴瘤-2(Bcl-2)表达降低。然而,MH处理对这些蛋白质有不同的影响;较低剂量增加,较高的剂量降低了表达。因此,较低剂量的MH可能参与受损肝细胞的处置。雌激素受体α(ERα)的表达也显示出与活性胱天蛋白酶3相似的趋势。此外,DEHP治疗后肿瘤坏死因子α(TNF-α)和核因子-κβ(NF-κβ)的表达上调,和MH处理下调这两种炎症标志物的表达。由于TNF-α和NF-κβ的下调与改善的肝功能对DEHP诱导的毒性一致,可以得出结论,MH介导的肝功能涉及TNF-α和NF-κβ的单个化。
Di-(2-ethylhexyl) phthalic acid (DEHP) pollutes the environment, and posing a significant risk to human and animal health. Consequently, a successful preventative strategy against DEHP-induced liver toxicity needs to be investigated. Morin hydrate (MH), a flavanol compound, possesses toxic preventive attributes against various environmental pollutants. However, the effects of MH have not been investigated against DEHP-induced liver toxicity. Female Swiss albino mice were divided into four groups: control, DEHP (orally administered with 500 mg/kg, DEHP plus MH 10 mg/kg, and DEHP plus MH 100 mg/kg for 14 days. The results showed that the MH treatment ameliorated the DEHP-induced liver dysfunctions by decreasing the alanine transaminase (ALT), aspartate aminotransferase (AST), total bilirubin, liver histoarchitecture, fibrosis, and markers of oxidative stress. Furthermore, DEHP increased apoptosis, increased active caspase 3 and decreased B cell lymphoma-2 (Bcl-2) expression. However, the MH treatment showed a differential effect on these proteins; a lower dose increased, and a higher dose decreased the expression. Thus, a lower dose of MH could be involved in the disposal of damaged hepatocytes. Expression of Estrogen receptors alpha (ERα) also showed a similar trend with active caspase 3. Furthermore, the expression of Tumor necrosis factor alpha (TNF-α) and Nuclear factor-κβ (NF-κβ) were up-regulated by DEHP treatment, and MH treatment down-regulated the expression of these two inflammatory markers. Since this down-regulation of TNF-α and NF-κβ coincides with improved liver functions against DEHP-induced toxicity, it can be concluded that MH-mediated liver function involves the singling of TNF-α and NF-κβ.