热休克蛋白70
肿瘤坏死因子α
高铁F1
热休克蛋白
热冲击
基因敲除
热休克蛋白90
化学
体内
热应力
细胞生物学
生物
生物化学
基因
免疫学
遗传学
动物科学
作者
Jingfei Jiang,Lei Fan,Zhiyi Yuan,Yugang Wang,Xinpei Wang,Xiaojin Yan,Xuan Yu,Dongming Xing,Lijun Du
标识
DOI:10.1016/s1875-5364(17)30034-1
摘要
Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.
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