Mechanism underlying berberine’s effects on HSP70/TNF α under heat stress: Correlation with the TATA boxes

Abstract

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 (TNF α). The exact mechanism underlying the HSP70 and TNF α 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 TNF α signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNF α and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNF α were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNF α were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNF α homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNF α. Furthermore, TNF α could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNF α 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.