BYAKANGELICIN,a main furanocoumarin constituent isolated and characterized as an aldose reductase inhibitor,and is effective for the treatment of sugar cataracts and diabetic neuropathy and hence might be useful as a lead compound for the development of new type drugs for clinical use.

在人类原代肝细胞中，byakangelicin 显著诱导了 CYP3A4 的表达，在 mRNA 水平约五倍，蛋白水平约三倍，但对人类孕烷X受体（hPXR）的表达没有影响。Byakangelicin 在浓度依赖的方式下激活了 CYP3A4 启动子（EC = 5 μM），且通过与 hPXR 共转染时，此激活作用得到了增强。CYP3A4 启动子中的 eNR4 结合元素对于 byakangelicin 诱导的 CYP3A4 转录激活是必需的[1]。

在大鼠饲以30%半乳糖饮食后，通过胃管给予byakangelicin 100 mg/kg的剂量连续14天，显著预防了白内障的形成和晶状体中半乳糖醇的积累。连续给药18天，发现该化合物能够抑制山梨醇积累，显著逆转链脲佐菌素诱导的糖尿病大鼠坐骨神经中肌醇含量的耗竭以及Na(+), K(+)ATP酶活性的下降。因此，在大鼠中byakangelicin 对治疗糖尿病性白内障和神经病变有效，可能作为开发临床新药的先导化合物[2]。

Cultures of human hepatocytes and a hepatoma cell line (Huh7 cells) were used.?mRNA and protein levels were measured by quantitative reverse transcription-polymerase chain reaction and Western blot.?Plasmid constructs and mutants were prepared by cloning and site-directed mutagenesis.?Reporter (luciferase) activity was determined by transient co-transfection experiments[1].

Induction of diabetes and drug treatment: Experimental diabetes was induced by a single injection of STZ (60 mg/kg), in 0.1 ml of 0.01 M citrate buffer (pH 4.5) into the tail vein of male Sprague-Dawley rats that had been fasted overnight.?Blood glucose was determined with a commercial blood glucose oxidase analysis kit.?Rats with blood glucose concentrations higher than 300 mg/dL were selected and considered to be diabetic.?Beginning with day 3 after the injection of STZ, diabetic rats were dosed with byakangelicin and epalrestat suspended in 5 g/dL gum arabic once a day throughout the experimental periods.?Controls and a group of normal rats were given the vehicle alone.?Animals were sacrificed by ether anesthesia and tissues were surgically removed, weighed and processed either for GC determination of polyol contents or for ATPase assay[2].