通过腹腔注射300 mg·kg-1氧嗪酸钾盐建立小鼠急性高尿酸血症模型,观察儿茶素单体对模型小鼠血清尿酸水平的影响;进一步进行血清、肝脏黄嘌呤氧化酶（XOD）活性实验和体外XOD抑制试验。结果显示,表儿茶素（EC）、表儿茶素没食子酸酯（ECG）和表没食子儿茶素（EGC）的灌胃剂量均为600 mg·kg-1时,在体内具有极显著降尿酸的作用,与模型对照组相比分别下降了23%（P<0.001）、35%（P<0.001）和37%（P<0.001）;ECG可降低小鼠血清和肝脏XOD活性,分别降低了31%（P<0.01）和32%（P<0.05）;在体外ECG和EGCG具有抑制XOD活性的作用。因此,EC、ECG和EGC具有降低高尿酸血症小鼠血清尿酸水平的作用,其中ECG的降尿酸效果与抑制小鼠体内XOD活性有关。
The mouse model of acute hyperuricemia was established by using 300 mg·kg-1 oxonic acid potassium salt to evaluate the influence of catechins on serum uric acid. The xanthine oxidase (XOD) activity in serum and liver and the inhibitory effect of catechins on XOD in vitro was further studied. Results showed that with dosage of 600 mg·kg-1, EC, ECG and EGC reduced the serum uric acid level in vivo significantly by 23% (P<0.001), 35% (P<0.001) and 37% (P<0.001), respectively compared with the model group. ECG could reduce XOD activity in serum and liver approximately by 31% (P<0.01) and 32% (P<0.05). In vitro, ECG and EGCG could inhibit XOD activity. Therefore EC, ECG and EGC could reduce the level of uric acid of hyperuricemia mice. The mechanism of uric acid lowering effect of ECG might be associated with its inhibitory effect on XOD.
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