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Potential roles of hepatic heat shock protein 25 and 70i in protection of mice against acetaminophen-induced liver injury

机译：肝热休克蛋白25和70i在保护小鼠免受对乙酰氨基酚引起的肝损伤中的潜在作用

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The aim of the present study was to assess the contribution of the level of expression of heat shock protein 25 (HSP25), 60 (HSP60), 70 (HSC70) and 70i (HSP70i) in mouse livers after a lethal dose of acetaminophen (APAP) to their survival. We examined changes in survival ratio, plasma APAP level and alanine aminotransferase (ALT) activity, and hepatic reduced glutathione (GSH), HSP25, HSP60, HSC70 and HSP70i levels following treatment of mice with APAP (500 mg/kg, p.o.). The plasma APAP level increased rapidly, and reached a maximum 0.5 h after APAP treatment. Hepatic GSH decreased rapidly, and was-almost completely depleted 1 h after APAP treatment. Plasma ALT activity, an index of liver injury, significantly increased from 3 h onwards after A-PAP treatment. The survival ratios 9 h, 24 h and 48 h after APAP treatment were 96%, 38% and 36%, respectively. We found a remarkable difference in the patterns of hepatic HSP25 and HSP70i induction in mice that survived after APAP treatment. HSP70i levels increased from 1 h onwards after APAP treatment in a time-dependent manner, and reached a maximum at 9 h. In contrast, HSP25 could be detected just 24 h after APAP treatment, and maximal accumulation was observed at 48 h. Other HSPs examined were unchanged. Notably, the survival ratio dropped by only 2% after HSP25 expression. Recently, a novel role for HSP25 as an anti-inflammatory factor was suggested. We have already shown that 48-h treatment with APAP induces severe centrilobular necrosis with inflammatory cell infiltration in mouse livers. Taken together, the level of expression of hepatic HSP25 may be a crucial determinant of the fate of mice exposed to APAP insult. (C) 2004 Elsevier Inc. All rights reserved. [References: 33]
机译：本研究的目的是评估致死剂量对乙酰氨基酚（APAP）后小鼠肝脏中热休克蛋白25（HSP25），60（HSP60），70（HSC70）和70i（HSP70i）的表达水平的贡献。 ）以求生存。我们用APAP（500 mg / kg，p.o.）处理小鼠后，检查了存活率，血浆APAP水平和丙氨酸氨基转移酶（ALT）活性以及肝还原型谷胱甘肽（GSH），HSP25，HSP60，HSC70和HSP70i水平的变化。血浆APAP水平迅速升高，并在APAP治疗后达到最大0.5 h。肝GSH迅速下降，APAP治疗后1小时几乎完全耗尽。 A-PAP治疗后3小时起，血浆ALT活性（一种肝损伤指标）显着增加。 APAP治疗后9小时，24小时和48小时的存活率分别为96％，38％和36％。我们发现APAP治疗后存活的小鼠肝HSP25和HSP70i诱导模式存在显着差异。从APAP治疗后的1小时起，HSP70i水平以时间依赖性的方式增加，并在9h达到最高。相比之下，APAP处理后仅24小时即可检测到HSP25，并且在48小时时观察到最大积累。所检查的其他HSP保持不变。值得注意的是，HSP25表达后，存活率仅下降了2％。最近，有人提出了HSP25作为抗炎因子的新作用。我们已经表明，用APAP治疗48小时会导致严重的小叶坏死，并在小鼠肝脏中引起炎性细胞浸润。两者合计，肝HSP25的表达水平可能是暴露于APAP损伤的小鼠命运的关键决定因素。 （C）2004 Elsevier Inc.保留所有权利。 [参考：33]

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