Fenpropathrin increases gliquidone absorption via causing damage to the integrity of intestinal barrier

Fenpropathrin is a commonly used pesticide, which was ingested by humans through diet and water. Gliquidone is a common hypoglycemic drug that diabetic patients need for long-term use. This study aimed to investigate the effects of long-term exposure to fenpropathrin on the intestinal barrier and intestinal absorption of the model drug gliquidone. The Ussing Chamber study had shown that fenpropathrin can increase the transport of gli-quidone in an isolated intestinal model. In addition, the intestinal absorption of fluorescein was significantly increased in fenpropathrin-exposed rats administered by gavage. Further research suggested that fenpropathrin exposure caused a series of pathological effects: the structure of the intestine was damaged, the expression of tight junction proteins in the intestinal tissue was decreased, the intestinal MDA was increased, the SOD was decreased, and the expression of inflammatory factors was increased. In the Caco-2 cell model, it was found that fenpropathrin can increase the transport of gliquidone in the Caco-2 cell monolayer, reduce the expression of tight junction proteins and increase reactive oxygen species in Caco-2 cells. Fenpropathrin exposure also resulted in decreasing expression of PPAR-gamma and UCP-2 in intestinal tissue and Caco-2 cell model, while causing increased expression of p-P38. The above results indicated that fenpropathrin exposure could induce oxidative stress and destroy the intestinal barrier by affecting the expression of p-P38/P38/PPAR-gamma/UCP-2 protein, thereby increasing the intestinal absorption of gliquidone. This study provides new insights into the hazards of fenpro-pathrin residues in the environment.

Automated summary

Long-term exposure to fenpropathrin may induce oxidative stress and disrupt the intestinal barrier, leading to increased intestinal absorption of gliquidone.