Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes.
10.1016/S1875-5364(17)30034-1
- Author:
Jing-Fei JIANG
1
;
Fan LEI
2
;
Zhi-Yi YUAN
1
;
Yu-Gang WANG
3
;
Xin-Pei WANG
1
;
Xiao-Jin YAN
1
;
Xuan YU
1
;
Dong-Ming XING
4
;
Li-Jun DU
5
Author Information
1. MOE (Ministry of Education) Key Laboratory of Protein Sciences, Laboratory of Molecular Pharmacology and Pharmaceutical Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
2. Department of Pharmacology and Pharmaceutical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
3. MD Anderson Cancer Center, University of Texas, Houston, TX 77030, USA.
4. MOE (Ministry of Education) Key Laboratory of Protein Sciences, Laboratory of Molecular Pharmacology and Pharmaceutical Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China. Electronic address: pharm@mail.tsinghua.edu.cn.
5. MOE (Ministry of Education) Key Laboratory of Protein Sciences, Laboratory of Molecular Pharmacology and Pharmaceutical Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China. Electronic address: lijundu@mail.tsinghua.edu.cn.
- Publication Type:Journal Article
- Keywords:
Berberine;
HSP70;
Hyperthermia;
TATA box;
TNFα
- MeSH:
Animals;
Berberine;
pharmacology;
HSP70 Heat-Shock Proteins;
genetics;
metabolism;
Heat Stress Disorders;
drug therapy;
genetics;
metabolism;
Hot Temperature;
Humans;
Male;
Mice;
Mice, Inbred ICR;
TATA Box;
drug effects;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
Chinese Journal of Natural Medicines (English Ed.)
2017;15(3):178-191
- CountryChina
- Language:English
-
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 (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.
