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首页> 外文期刊>Molecular pharmacology. >Induction of overexpression of the 27- and 70-kDa heat shock proteins by bicyclol attenuates concanavalin A-Induced liver injury through suppression of nuclear factor-kappaB in mice.
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Induction of overexpression of the 27- and 70-kDa heat shock proteins by bicyclol attenuates concanavalin A-Induced liver injury through suppression of nuclear factor-kappaB in mice.

机译：双环醇诱导27 kDa和70 kDa热休克蛋白的过表达通过抑制小鼠中的核因子kappaB减弱了伴刀豆球蛋白A引起的肝损伤。

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Heat shock proteins (HSPs) are molecular chaperones critical for cell survival under adverse environmental conditions and for normal cellular homeostasis. Bicyclol, a novel antihepatitis drug, has been shown to protect against liver injury in animals. However, it is unclear how bicyclol protects against liver injury. We recently found that bicyclol is an inducer of HSPs. We wondered whether bicyclol regulated the expression of HSPs to produce a liver protection in vivo. Thus, this study was designed to address these questions using a mouse model with concanavalin A (ConA)-induced liver injury. Oral administration of bicyclol markedly alleviated ConA-caused liver injury in mice as indicated by the reduction of serum aminotransferases, liver necrosis, and the release of cytochrome c and apoptosis-inducing factor from mitochondria and hepatic DNA fragmentation. Correlated with this, bicyclol induced the increase of mRNA and protein levels of hepatic 27- and 70-kDa HSPs (HSP27 and HSP70) in the mice. Correspondingly, the elevated HSP27 and HSP70 suppressed inhibitor kappaB degradation and nuclear factor kappaB (NF-kappaB) activation that were caused by ConA. The protective effects of bicyclol on ConA-induced mouse liver injury were markedly attenuated by quercetin, an inhibitor of HSPs synthesis. Our results suggest that the antihepatitis drug bicyclol may protect against liver injury by inducing the expression of hepatic HSP27 and HSP70 and consequently inhibit the transcription factor NF-kappaB-mediated apoptosis and necrosis in liver tissue.
机译：热休克蛋白（HSP）是分子伴侣，对于在不利环境条件下的细胞存活和正常的细胞稳态至关重要。双环醇是一种新型的抗肝炎药物，已被证明可以保护动物免受肝损伤。但是，尚不清楚双环化合物如何预防肝损伤。我们最近发现双环醇是HSP的诱导剂。我们想知道双环酚是否在体内调节HSP的表达以产生肝脏保护作用。因此，本研究旨在使用伴刀豆球蛋白A（ConA）引起的肝损伤的小鼠模型来解决这些问题。口服双环酚可显着减轻ConA引起的小鼠肝损伤，如血清氨基转移酶的减少，肝坏死以及线粒体中细胞色素c和凋亡诱导因子的释放以及肝DNA片段化所表明的。与此相关的是，双环醇诱导了小鼠肝脏27kDa和70kDa HSP（HSP27和HSP70）的mRNA和蛋白质水平的增加。相应地，升高的HSP27和HSP70抑制了由ConA引起的抑制剂kappaB降解和核因子kappaB（NF-kappaB）活化。槲皮素（一种HSPs合成抑制剂）显着减弱了双环醇对ConA诱导的小鼠肝损伤的保护作用。我们的结果表明，抗肝炎药物双环醇可通过诱导肝HSP27和HSP70的表达来预防肝损伤，从而抑制转录因子NF-κB介导的肝细胞凋亡和坏死。

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