期刊论文详细信息
BMC Veterinary Research
Inhibition of heat-induced apoptosis in rat small intestine and IEC-6 cells through the AKT signaling pathway
Shining Guo1  Jianqin Xu3  Tao Liu2  Hong Zhao2  Xiaoxi Liu2  Shasha He3  Changrong Wan3  Peng Yin3  Fenghua Liu2  Zhimin Gao1 
[1] College of Veterinary Medicine, South China Agricultural University, Tianhe, Guangzhou, Guangdong 510642, R. P China;Department of Animal Science and Technology, Beijing University of Agriculture, Beijing 102206, P. R China;College of Veterinary Medicine, China Agricultural University, No. 2, West Yuanmingyuan Road, Beijing 100193, P. R China
关键词: Rat;    IEC-6 cells;    Small intestine;    AKT;    Apoptosis;    Heat stress;   
Others  :  1119397
DOI  :  10.1186/1746-6148-9-241
 received in 2013-10-11, accepted in 2013-11-25,  发布年份 2013
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【 摘 要 】

Background

As the world warms up, heat stress is becoming a major cause of economic loss in the livestock industry. Long-time exposure of animals to hyperthermia causes extensive cell apoptosis, which is harmful to them. AKT and AKT-related serine–threonine kinases are known to be involved in signaling cascades that regulate cell survival, but the mechanism remains elusive. In the present study, we demonstrate that phosphoinositide 3-kinase (PI3K) /AKT signal pathway provides protection against apoptosis induced by heat stress to ascertain the key point for treatment.

Results

Under heat stress, rats showed increased shedding of intestinal epithelial cells. These rats also had elevated levels of serum cortisol and improved expression of heat shock proteins (Hsp27, Hsp70 and Hsp90) in response to heat stress. Apoptosis analysis by TUNEL assay revealed a higher number of villi epithelial cells that were undergoing apoptosis in heat-treated rats than in the normal control. This is supported by gene expression analysis, which showed an increased ratio of Bax/Bcl-2 (p < 0.05), an important indicator of apoptosis. During heat-induced apoptosis, more AKTs were activated, showing increased phosphorylation. An increase of BAD phosphorylation, which is an inhibitory modification, ensued. In rat IEC-6 cell line, a significant higher level of AKT phosphorylation was observed at 2 h after heat exposure. This coincided with a marked reduction of apoptosis.

Conclusion

Together, these results suggest that heat stress caused damages to rat jejunum and induced apoptosis to a greater degree. HSPs and pro-survival factors were involved in response to heat stress. Among them, AKT played a key role in inhibiting heat-induced apoptosis.

【 授权许可】

   
2013 Gao et al.; licensee BioMed Central Ltd.

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