Irreversible electroporation (IRE) is a newly developed non-thermal ablative therapy. During the IRE procedure, the permeability of the cell membrane is irreversibly changed by application of high-energy pulses across the tissue. This induces the breakdown of cell homeostasis, and thereby cell death. Here, we present an in vivo study to demonstrate IRE ablation of gastric tissue and characterize the changes that occur with time therein. No significant complications were observed in the test rats during the experiment. The electroporated tissues exhibited apoptosis at 10, 24 and 48 h after IRE ablation. The apoptosis peaked at 10 h after IRE and then declined, suggesting that the ablated tissue rapidly recovered owing to intense metabolic activity. In addition, the electroporated tissues exhibited morphological changes such as pyknosis and karyorrhexis, while histological analysis showed that the blood vessels were preserved. Interestingly, electroporation greatly affected the mucosa and muscularis propria, but not the submucosa and serosa. This study suggests that IRE could potentially be used as a minimally invasive treatment for early gastric cancer that does not exhibit lymph node metastasis or dysplasia.

Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown. Here, we investigated the role of exosomes in NAFLD progression. Exosomes were isolated from a human hepatoma cell line treated with palmitic acid (PA) and their miRNA profiles examined by microarray. The human hepatic stellate cell (HSC) line (LX-2) was then treated with exosome isolated from hepatocytes. Compared with controls, PA-treated hepatocytes displayed significantly increased CD36 and exosome production. The microarray analysis showed there to be distinctive miRNA expression patterns between exosomes from vehicle- and PA-treated hepatocytes. When LX-2 cells were cultured with exosomes from PA-treated hepatocytes, the expression of genes related to the development of fibrosis were significantly amplified compared to those treated with exosomes from vehicle-treated hepatocytes. In conclusion, PA treatment enhanced the production of exosomes in these hepatocytes and changed their exosomal miRNA profile. Moreover, exosomes derived from PA-treated hepatocytes caused an increase in the expression levels of fibrotic genes in HSCs. Therefore, exosomes may have important roles in the crosstalk between hepatocytes and HSCs in the progression from simple steatosis to NASH.