Abstract
Heat-stress exposure increased the expression of heat-shock proteins (HSPs), B-cell lymphoma 2 (BCL-2) and anti-oxidative enzymes to maintain normal cellular function by attenuating the oxidative reaction and apoptosis. Reducing the stress response or enhancing anti-stress capability is an important goal in animal production. Our previous study indicated a protective role of flavangenol, a pine bark extract, in chicks after three hours of high-temperature exposure. However, the cellular mechanism of flavangenol was not clarified ex vivo. In the current study, we investigated the effect of flavangenol on cellular apoptosis and oxidation in heat-stressed treated chick brain cells (mixed neurons and glia cells). The primary brain cells were isolated from the diencephalon of 14-day-old chicks and cultured at 41.5 °C (to mimic the body temperature of young chicks), and were treated with flavangenol from day 3 of isolation to day 8. Cells were kept bathed in the cell culture dish under a high temperature (HT: 45 °C, 20 or 60 min) on day 8 and were then collected for analysis of cell viability as well as for HSP and other related gene expression. Flavangenol treatment significantly increased cell viability and BCL-2 mRNA expression, and attenuated HSP-70 and BCL-2-associated X protein mRNA expression. Moreover, flavangenol treatment elevated the mRNA expression of glutathione peroxidase in the HT group, which indicates that cellular anti-oxidative ability was strengthened by flavangenol. In conclusion, flavangenol may play a protective role in cells damaged or killed by heat stress by increasing cellular anti-oxidative pathways.
| Original language | English |
|---|---|
| Pages (from-to) | 1-11 |
| Number of pages | 11 |
| Journal | Journal of Thermal Biology |
| Volume | 81 |
| DOIs | |
| Publication status | Published - Apr 1 2019 |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Physiology
- Agricultural and Biological Sciences(all)
- Developmental Biology
Cite this
Flavangenol regulates gene expression of HSPs, anti-apoptotic and anti-oxidative factors to protect primary chick brain cells exposed to high temperature. / Yang, Hui; Surchowdhury, Vishwajit; Han, Guofeng; Zhang, Rong; Furuse, Mitsuhiro.
In: Journal of Thermal Biology, Vol. 81, 01.04.2019, p. 1-11.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Flavangenol regulates gene expression of HSPs, anti-apoptotic and anti-oxidative factors to protect primary chick brain cells exposed to high temperature
AU - Yang, Hui
AU - Surchowdhury, Vishwajit
AU - Han, Guofeng
AU - Zhang, Rong
AU - Furuse, Mitsuhiro
PY - 2019/4/1
Y1 - 2019/4/1
N2 - Heat-stress exposure increased the expression of heat-shock proteins (HSPs), B-cell lymphoma 2 (BCL-2) and anti-oxidative enzymes to maintain normal cellular function by attenuating the oxidative reaction and apoptosis. Reducing the stress response or enhancing anti-stress capability is an important goal in animal production. Our previous study indicated a protective role of flavangenol, a pine bark extract, in chicks after three hours of high-temperature exposure. However, the cellular mechanism of flavangenol was not clarified ex vivo. In the current study, we investigated the effect of flavangenol on cellular apoptosis and oxidation in heat-stressed treated chick brain cells (mixed neurons and glia cells). The primary brain cells were isolated from the diencephalon of 14-day-old chicks and cultured at 41.5 °C (to mimic the body temperature of young chicks), and were treated with flavangenol from day 3 of isolation to day 8. Cells were kept bathed in the cell culture dish under a high temperature (HT: 45 °C, 20 or 60 min) on day 8 and were then collected for analysis of cell viability as well as for HSP and other related gene expression. Flavangenol treatment significantly increased cell viability and BCL-2 mRNA expression, and attenuated HSP-70 and BCL-2-associated X protein mRNA expression. Moreover, flavangenol treatment elevated the mRNA expression of glutathione peroxidase in the HT group, which indicates that cellular anti-oxidative ability was strengthened by flavangenol. In conclusion, flavangenol may play a protective role in cells damaged or killed by heat stress by increasing cellular anti-oxidative pathways.
AB - Heat-stress exposure increased the expression of heat-shock proteins (HSPs), B-cell lymphoma 2 (BCL-2) and anti-oxidative enzymes to maintain normal cellular function by attenuating the oxidative reaction and apoptosis. Reducing the stress response or enhancing anti-stress capability is an important goal in animal production. Our previous study indicated a protective role of flavangenol, a pine bark extract, in chicks after three hours of high-temperature exposure. However, the cellular mechanism of flavangenol was not clarified ex vivo. In the current study, we investigated the effect of flavangenol on cellular apoptosis and oxidation in heat-stressed treated chick brain cells (mixed neurons and glia cells). The primary brain cells were isolated from the diencephalon of 14-day-old chicks and cultured at 41.5 °C (to mimic the body temperature of young chicks), and were treated with flavangenol from day 3 of isolation to day 8. Cells were kept bathed in the cell culture dish under a high temperature (HT: 45 °C, 20 or 60 min) on day 8 and were then collected for analysis of cell viability as well as for HSP and other related gene expression. Flavangenol treatment significantly increased cell viability and BCL-2 mRNA expression, and attenuated HSP-70 and BCL-2-associated X protein mRNA expression. Moreover, flavangenol treatment elevated the mRNA expression of glutathione peroxidase in the HT group, which indicates that cellular anti-oxidative ability was strengthened by flavangenol. In conclusion, flavangenol may play a protective role in cells damaged or killed by heat stress by increasing cellular anti-oxidative pathways.
UR - http://www.scopus.com/inward/record.url?scp=85061443939&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85061443939&partnerID=8YFLogxK
U2 - 10.1016/j.jtherbio.2019.02.010
DO - 10.1016/j.jtherbio.2019.02.010
M3 - Article
C2 - 30975405
AN - SCOPUS:85061443939
VL - 81
SP - 1
EP - 11
JO - Journal of Thermal Biology
JF - Journal of Thermal Biology
SN - 0306-4565
ER -