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适当的热休克预处理可减轻四氯化碳诱导的小鼠急性肝损伤,并加速肝脏修复。

Proper heat shock pretreatment reduces acute liver injury induced by carbon tetrachloride and accelerates liver repair in mice.

作者信息

Li San-Qiang, Wang Dong-Mei, Shu You-Ju, Wan Xue-Dong, Xu Zheng-Shun, Li En-Zhong

机构信息

Molecular Medicine Key Laboratory of Liver Injury and Repair, Medical College, Henan University of Science and Technology, An hui road 31, Jian xi district, Luoyang 471003, P.R. China.

Department of Environmental Engineering and Chemistry, Luoyang Insititute of Science and Technology, Wang cheng road 90, Luo long district, Luoyang 471023, P.R. China.

出版信息

J Toxicol Pathol. 2013 Dec;26(4):365-73. doi: 10.1293/tox.2013-0006. Epub 2013 Dec 26.

Abstract

Whether proper heat shock preconditioning can reduce liver injury and accelerate liver repair after acute liver injury is worth study. So mice received heat shock preconditioning at 40°C for 10 minutes (min), 20 min or 30 min and recovered at room temperature for 8 hours (h) under normal feeding conditions. Then acute liver injury was induced in the heat shock-pretreated mice and unheated control mice by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl4). Hematoxylin and eosin (H&E) staining, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and the expression levels of heat shock protein 70 (HSP70), cytochrome P450 1A2 (CYP1A2) and proliferating cell nuclear antigen (PCNA) were detected in the unheated control mice and heat shock-pretreated mice after CCl4 administration. Our results showed that heat shock preconditioning at 40°C for 20 min remarkably improved the mice's survival rate (P<0.05), lowered the levels of serum AST and ALT (P<0.05), induced HSP70 (P<0.01), CYP1A2 (P<0.01) and PCNA (P<0.05) expression, effectively reduced liver injury (P<0.05) and accelerated the liver repair (P<0.05) compared with heat shock preconditioning at 40°C for 10 min or 30 min in the mice after acute liver injury induced by CCl4 when compared with the control mice. Our results may be helpful in further investigation of heat shock pretreatment as a potential clinical approach to target liver injury.

摘要

适当的热休克预处理能否减轻急性肝损伤后的肝损伤并加速肝修复值得研究。因此,将小鼠在40°C下进行10分钟、20分钟或30分钟的热休克预处理,并在正常饲养条件下于室温恢复8小时。然后通过腹腔注射四氯化碳(CCl4)在热休克预处理的小鼠和未加热的对照小鼠中诱导急性肝损伤。在给予CCl4后,检测未加热的对照小鼠和热休克预处理小鼠的苏木精和伊红(H&E)染色、血清天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)水平以及热休克蛋白70(HSP70)、细胞色素P450 1A2(CYP1A2)和增殖细胞核抗原(PCNA)的表达水平。我们的结果表明,与在40°C下进行10分钟或30分钟热休克预处理的小鼠相比,在由CCl4诱导急性肝损伤的小鼠中,40°C下20分钟的热休克预处理显著提高了小鼠的存活率(P<0.05),降低了血清AST和ALT水平(P<0.05),诱导了HSP70(P<0.01)、CYP1A2(P<0.01)和PCNA(P<0.05)的表达,有效减轻了肝损伤(P<0.05)并加速了肝修复(P<0.05)。我们的结果可能有助于进一步研究热休克预处理作为一种潜在的针对肝损伤的临床方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac4c/3921919/eeb8d618b710/tox-26-365-g001.jpg

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