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在酪氨酸诱导的小鼠肝损伤模型上观察到50000U／kg的白细胞介素-1β（IL－1β），分别提前1，6和12h腹腔注射，可不同程度地降低GPT和GOT漏出，其中以提前12h的效果最强，而在给予醋氨酸之后1h再注射此素则无效。在提前12h这一时间点观察不同剂量（1000，30000，50000U/kg）IL－1β作用的结果表明，IL－1β抑制酪氨酚诱导的转氨酶漏出呈一定的剂量-效应关系，这三个剂量还可不同程度地降低小鼠死亡率。IL-1β受体拮抗剂可阻断IL－1β的保护作用。对IL－1β肝细胞保护作用机制的初步分析表明，IL-1β可增加正常肝细胞还原型谷胱甘肽（GSH）含量并阻止醋氨酸诱导的GSH含量的降低和氧化型谷优甘肽（GSSG）的增加，此外还可降低酪氨酚诱导的肝脏丙二醛（Malondiadehyde，MDA）含量的增加。结果表明，IL-1β可预防酪氨酸诱导的肝损伤，可能由IL－1β受体所介导，可能与增加谷胱甘肽合成和降低肝脏脂质过氧化有关。
50000U / kg interleukin-1β (IL-1β) was observed on the tyrosine-induced mouse liver injury model, which was injected intraperitoneally 1, 6 and 12 h respectively, which could reduce the GPT and GOT leakage to some extent, The effect of 12h ahead of the strongest, but after the administration of acetic acid 1h injection of this hormone is invalid. The results of observing the effect of IL-1β at different doses (1000, 30000, 50000U / kg) at the time of 12h earlier showed that IL-1β inhibited the tyrosine-induced transaminase leakage in a dose-dependent manner. Can also reduce the mortality of mice to varying degrees. IL-1β receptor antagonists can block the protective effect of IL-1β. Preliminary analysis of the mechanism of protective effect of IL-1β hepatocytes showed that IL-1β can increase the content of reduced glutathione (GSH) in normal hepatocytes and prevent the decrease of glutathione-induced GSH level and oxidative glutathione (GSSG) increase, in addition to reducing tyrosine-induced liver malondialdehyde (Malondiadehyde, MDA) increased. The results showed that IL-1β could prevent tyrosine-induced liver injury, which may be mediated by IL-1β receptor, which may be related to increasing glutathione synthesis and reducing hepatic lipid peroxidation.