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冷应激对B6C3F1和ICR小鼠对乙酰氨基酚诱导的肝损伤的抑制作用。

Inhibitory effect of cold stress against acetaminophen-induced hepatic injury in B6C3F1 and ICR mice.

作者信息

Yamamoto H, Fujii K, Hayakawa T

机构信息

Department of Environmental Medicine, University of Tsukuba, Ibaraki, Japan.

出版信息

Toxicol Lett. 1995 Nov 15;81(2-3):125-30. doi: 10.1016/0378-4274(95)03424-2.

Abstract

The effect of cold stress (at 0 +/- 1 degree C for 3 h) on acetaminophen-induced hepatic injury was investigated in B6C3F1 and ICR mice. When acetaminophen (250 mg/kg) was injected intraperitoneally in B6C3F1 mice, the plasma GPT activity was significantly increased by 93 or 107-fold at 6 h or 24 h after the drug injection. However, when B6C3F1 mice were exposed to cold stress, the increase in plasma GPT activity induced by acetaminophen was significantly inhibited by 53% and 44%, respectively. On the other hand, when acetaminophen at the same dose was injected in ICR mice, the activity of plasma GPT was increased by 9-fold at 6 h, or 16-fold at 24 h after the drug injection. The increased plasma GPT activity elicited a significant inhibition of 35% and 36%, respectively, by the exposure to cold stress. These results suggest that acetaminophen-induced hepatic injury may be blocked by physical stress in mice.

摘要

研究了冷应激(在0±1℃下3小时)对B6C3F1和ICR小鼠对乙酰氨基酚诱导的肝损伤的影响。当在B6C3F1小鼠腹腔注射乙酰氨基酚(250mg/kg)后,在注射药物后6小时或24小时,血浆谷丙转氨酶(GPT)活性显著增加93倍或107倍。然而,当B6C3F1小鼠暴露于冷应激时,乙酰氨基酚诱导的血浆GPT活性增加分别被显著抑制了53%和44%。另一方面,当在ICR小鼠中注射相同剂量的乙酰氨基酚时,在注射药物后6小时血浆GPT活性增加9倍,24小时增加16倍。冷应激分别使增加的血浆GPT活性显著抑制了35%和36%。这些结果表明,在小鼠中,物理应激可能会阻断乙酰氨基酚诱导的肝损伤。

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