Liver Unit, Hebrew University-Hadassah Medical Center, Jerusalem, Israel.
J Dig Dis. 2013 Feb;14(2):84-92. doi: 10.1111/1751-2980.12003.
To determine the metabolic and immunological effects of the oral administration of DT56a, an enzymatic isolate of soybeans.
DT56a was orally administered to mice in three animal models: leptin deficiency, high-fat diet (HFD) supplementation and immune-mediated hepatitis. Liver damage and immunological status were assessed.
Oral administration of DT56a to leptin-deficient (ob/ob) and HFD mice led to a significant reduction in serum triglyceride (TG) and total cholesterol (TC) levels. DT56a-treated mice in both models exhibited a significant reduction in hepatic levels of TG and marked alleviation of glycemic control as indicated by significant decreases in fasting blood glucose levels and glucose tolerance tests. The levels of liver enzymes were reduced. These metabolic effects were associated with altered distributions of regulatory T (Tregs) and natural killer T (NKT) cells. DT56a suppressed the immune-mediated liver damage induced by concanavalin A indicated by decreased liver enzymes and serum interferon-γ levels and by improved histology and decreased hepatic apoptosis. Oral administration of DT56a also alleviated immune-mediated hepatitis and affected Tregs and NKT cells.
Oral administration of DT56a promotes a hepatoprotective effect associated with an alteration in the distribution of Tregs and NKT cells.
确定口服 DT56a(大豆的一种酶分离物)的代谢和免疫作用。
将 DT56a 口服给予三种动物模型中的小鼠:瘦素缺乏、高脂肪饮食(HFD)补充和免疫介导性肝炎。评估肝损伤和免疫状态。
口服 DT56a 给瘦素缺乏(ob/ob)和 HFD 小鼠导致血清甘油三酯(TG)和总胆固醇(TC)水平显著降低。两种模型中的 DT56a 治疗小鼠均表现出肝 TG 水平的显著降低,以及血糖控制的明显改善,表现为空腹血糖水平和葡萄糖耐量试验显著降低。肝酶水平降低。这些代谢作用与调节性 T(Treg)和自然杀伤 T(NKT)细胞分布的改变有关。DT56a 抑制了由伴刀豆球蛋白 A 诱导的免疫介导性肝损伤,表现为肝酶和血清干扰素-γ水平降低,组织学改善和肝凋亡减少。口服 DT56a 还缓解了免疫介导性肝炎,并影响了 Treg 和 NKT 细胞。
口服 DT56a 可促进肝保护作用,与 Treg 和 NKT 细胞分布的改变有关。