Research on Mechanism of Superparamagnetic Iron Oxide Nanoparticles in Activating Endoplasmic Reticulum and Prompting Apoptosis of Liver Cells Through Mediation of Tumor Necrosis Factor-α/Tumor Necrosis Factor Receptor 1 (TNF-α/TNFR1) Pathway

Author:

Zhou Liyang1,He Qin1,Yang Xiaoàn2,Zheng Shuo1,Ou Xueting1

Affiliation:

1. Department of Infectious Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510150, China

2. Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China

Abstract

The aim of this study was to assess mechanism of superparamagnetic iron oxide nanoparticles (SPIO-NPs) in activating endoplasmic reticulum (ER) and prompting apoptosis of liver cells through mediating the TNF-α/TNFR1 pathway. The SPIO-NPs were prepared and identified, and HegG2 cells were cultivated in vitro, and their apoptosis was detected. The specific pathogen-free (SPF)-grade rats were divided into several groups; which included blank group, low concentration group, high concentration group and control group. The enzymatic activity of Caspase-3 in liver tissue was tested, and expressions of Caspase-3, Bax, Bcl-2, TNF-α, p-TNFR1, IRE1α, and eIF2α were tested. The size of prepared SPIO-NPs was 7.5 nm and there was no coagulation. There was good dispersity and electric potential, and appearance was stable. The apoptotic rate in the high concentration group was notably higher than in the other groups. There was notable inflammatory cell infiltration in the high concentration group, where quantity of apoptosis was highest. The quantity of apoptosis and fluorocyte in the high concentration group were notably higher than in the other groups. Moreover, there were over expressions of Caspase-3, Bax, Caspase-3, p-TNFR1, IRE1α, and eIF2α in the high concentration group while the expression of TNF-α was lowest. The apoptosis of HegG2 cells was prompted by SPIO-NPs, and quantity of apoptosis was increased with increased adopted concentration. The active expression of p-TNFR1, IRE1α, and eIF2α could be prompted to reduce the expression of TNF-α and increase the expression of Caspase-3 and Bax for prompting the apoptosis.

Publisher

American Scientific Publishers

Subject

Pharmaceutical Science,General Materials Science,Biomedical Engineering,Medicine (miscellaneous),Bioengineering

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