RETRACTED: Amorphous Selenium Nanoparticles Improve Vascular Function in Rats With Chronic Isocarbophos Poisoning via Inhibiting the Apoptosis of Vascular Endothelial Cells

• Published in: Frontiers in bioengineering and biotechnology Vol. 9
• Main Authors: Zhu, Moli, Gao, Zhitao, Fu, Yutian, Qiu, Yue, Huang, Keke, Zhu, Chaonan, Wu, Yinan, Zhu, Tiantian, Wang, Qianqian, Yang, Lin, Yin, Yaling, Li, Peng
• Format: Journal Article
• Language: English
• Published: Frontiers Media S.A 24-06-2021
• Subjects: amorphous selenium nanoparticles; apoptosis; human umbilical vein endothelial cells; isocarbophos; sodium hydrogen exchanger 1; vascular dysfunction
• ISSN: 2296-4185; 2296-4185
• DOI: 10.3389/fbioe.2021.673327

Aim This study aimed to investigate the preventive effect and possible mechanism of amorphous selenium nanoparticles (A-SeQDs) on isocarbophos induced vascular dysfunction. Methods A-SeQDs was made by auto redox decomposition of selenosulfate precursor. Male rats were given isocarbophos (0.5 mg/kg/2 days) by intragastric administration for 16 weeks to induce vascular dysfunction. During the course, A-SeQDs (50 mg/kg/day) was added to the water from week 5. Then, the rats were killed to observe and test the influence of A-SeQDs on the vascular dysfunction induced by isocarbophos. Finally, human umbilical vein endothelial cells (HUVECs) were treated with 10% DMEM of isocarbophos (100 μM) for 5 days to detect the related indexes. Before the use of isocarbophos treatment, different drugs were given. Results A-SeQDs could reduce total carbon dioxide, MDA, VCAM-1, ICAM-1, IL-1, and IL-6 while increasing oxygen saturation, NO content, and SOD activity in rats. A-SeQDs also resulted in relatively normal vascular morphology, and the expression of sodium hydrogen exchanger 1 (NHE1) and caspase-3 decreased in rats. Furthermore, in HUVECs treated with isocarbophos, A-SeQDs maintained mitochondrial membrane potential, inhibited the cleaved caspase-3 expression, and released cytochrome c from mitochondria to cytosol. Conclusion A-SeQDs can inhibit the apoptosis of HUVECs through the mitochondrial pathway, and effectively treat the impairment of vascular endothelial function caused by isocarbophos, which is NHE1-dependent.