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2,3,7,8-tetrachlorodibenzo-p-dioxin inhibits autophagy via Akt/ mTOR signaling pathway in RAW 264.7 macrophages
Jing Lu,Meitong Liu,Haochen Zheng,Yong Fan,Qian Zhang,Shuang Guan *
College of Food Science and Engineering, Jilin University, 130062
*Correspondence author
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Funding: National Natural Science Foundation of China (No.31540049), National College Students Innovation and Entrepreneurship Training Program of China(No.201910183315)
Opened online:26 October 2020
Accepted by: none
Citation: Jing Lu,Meitong Liu,Haochen Zheng.2,3,7,8-tetrachlorodibenzo-p-dioxin inhibits autophagy via Akt/ mTOR signaling pathway in RAW 264.7 macrophages[OL]. [26 October 2020] http://en.paper.edu.cn/en_releasepaper/content/4752932
 
 
2,3,7,8-tetrachlorodibenzodioxine (TCDD) was a highly toxic contamination and detected in the environment and food. It can be bio-magnified through food chain and bio-accumulate in human bodies, then cause various adverse health effects. Autophagy was a self-regulating process that degraded proteins and organelles in cells. The disruptions of autophagy balance have been bound up with multiple diseases and metabolic processes. In this paper, we detected the effects of TCDD on autophagy in RAW 264.7 cells and traced the molecular mechanism. The results showed that TCDD dose-dependently inhibited autophagy with the range from 0 to 10nM. Further, we found that this inhibition of autophagy was due to the decrease of p-Akt/Akt and increase of p-mTOR/mTOR expression. In addition, the autophagy inhibition caused by TCDD was resumed by using reversible mTOR inhibitor (rapamycin) and a selective Akt inhibitor (LY294002). This evidence showed that Akt/mTOR signaling pathway plays an important role in the autophagy induced by TCDD in RAW 264.7 cells. Our study confirmed the autophagy injury of TCDD on RAW 264.7 macrophages and the mechanism of TCDD toxicity was supplemented at the molecular level.
Keywords:2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); Autophagy; Macrophages; Akt/mTOR
 
 
 

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