Development of preventive and therapeutic method of asthma by the regulation of arginase

我们通过接种抗il -13单克隆抗体和精氨酸酶抑制剂，证明了在尘螨诱导的小鼠哮喘模型中，作为支气管扩张剂的一氧化氮的缺失是导致精氨酸消耗和精氨酸酶上调的一氧化氮合酶产生的一氧化氮减少的原因。此外，研究表明，在人类哮喘中，血清精氨酸酶水平升高调节血清精氨酸水平和呼出一氧化氮。

We demonstrated that the deletion of nitric oxide as a bronchodilator in asthma was contributed to consumption of arginine and low generation of nitric oxide from nitric oxide synthase from upregulated arginase in mite-induced mice asthma model by inoculation of anti-IL-13 monoclonal antibody and an arginase inhibitor. Moreover, it was demonstrated that in human asthma increased serum arginase levels regulated serum arginine levels and exhaled nitric oxide.