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Published on: January 11, 2019
Sodium Ion Channel Active Agent Deltamethrin Induces Cell Apoptosis and Cell Cycle Arrest through Mitochondrial
Xiaohua Wang1, Wanlin Shen2, Tian Tian1
1Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Nanjing Medical University (Changzhou Second People's Hospital), Changzhou 213000, Jiangsu, China.
Introduction:
Pulmonary Fibrosis (PF) is a common outcome of many interstitial lung diseases. Sodium ion channels play an important role in maintaining membrane potential, transmitting ion signals across the membrane, and mediating cell proliferation/migration. Deltamethrin (DM) can prevent the closure of voltage-gated sodium ion channels in insect axon membranes. This study aimed to further evaluate the potential effects of DM on Human Fetal Lung Fibroblasts (HFLF).
Methods:
The characteristic apoptotic changes were also assessed using DNA fragmentation analysis, terminal deoxynucleotidyl Transferase-Mediated Dutp Nick End Labeling (TUNEL), and annexin V/PI and Hoechst 33342/PI double staining. In addition, DM-induced cell cycle arrest in the G0/G1 phase was detected in a dosedependent manner. Furthermore, transcriptional and translational expression of selected genes under DM stress were used to confirm the analysis.
Results:
We showed that DM dose-dependently decreased cell viability and inhibited cell proliferation in the HFLF cell line. The data suggested that the effect of DM inhibition was at least partly through regulating the expression of Ras, p53, p21, p27, cyclin D1, cytochrome c, caspase-3, and Bcl-2 family members.
Discussion:
These results revealed that DM might induce cell apoptosis and cell cycle arrest through a mitochondrial-dependent cytotoxic stress pathway in the HFLF cell line, but there is a lack of animal experiments to verify this. We will continue to follow up on the experiment to further improve it.
Conclusion:
Our study provides insight into assessing the potential anti-pulmonary fibrosis function of DM at the molecular level.
