Flavangenol regulates gene expression of HSPs, anti-apoptotic and anti-oxidative factors to protect primary chick brain cells exposed to high temperature

Hui Yang, Vishwajit Surchowdhury, Guofeng Han, Rong Zhang, Mitsuhiro Furuse

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)1-11
Number of pages11
JournalJournal of Thermal Biology
Volume81
DOIs
Publication statusPublished - Apr 1 2019

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Heat-Shock Proteins
heat shock proteins
Gene expression
Brain
chicks
brain
Gene Expression
gene expression
lymphoma
Temperature
B-lymphocytes
temperature
B-Cell Lymphoma
cell viability
heat stress
cells
apoptosis
Hot Temperature
Cells
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Agricultural and Biological Sciences(all)
  • Developmental Biology

Cite this

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title = "Flavangenol regulates gene expression of HSPs, anti-apoptotic and anti-oxidative factors to protect primary chick brain cells exposed to high temperature",
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.",
author = "Hui Yang and Vishwajit Surchowdhury and Guofeng Han and Rong Zhang and Mitsuhiro Furuse",
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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.

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