Inhibition of the Nrf2/p38MAPK pathway involved in deltamethrin-induced apoptosis and fibrosis in quail kidney

Deltamethrin (DLM) is a broad-spectrum and effective pyrethroid insecticide. However, DLM has good residual activity on most surfaces and many insects, so it poses a threat to the environment and health of animals and human. Exposure to DLM can cause kidney injury, but the mechanism is not well understood. Therefore, we investigated the possible mechanism of quail kidney injury induced by chronic exposure to different doses of DLM for 12 weeks. The results showed that chronic exposure to DLM induced apoptosis and fibrosis of quail kidney through the promotion of oxidative stress by down-regulating nuclear factor erythroid 2 related factor 2 (Nrf2), up-regulating the phosphorylation of p38 mitogen-activated protein kinases (p38MAPK). Furthermore, DLM-induced kidney apoptosis in quails as evidenced by increased expression of B-cell lymphoma gene 2-associated X while decreased expression of B-cell lymphoma-extra large. Simultaneously, DLM-induced kidney fibrosis in quails as evidenced by increased expression of fibrosis maker proteins. Overall, the results demonstrate that chronic DLM exposure induces kidney apoptosis and fibrosis via inhibition of the Nrf2/p38MAPK pathway. This study provides a new understanding for the mechanism of DLM-induced quail kidney injury and also provides a theoretical basis for treatment of the DLM poisoning.

Automated summary

Deltamethrin (DLM) is an effective pyrethroid insecticide with broad-spectrum activity, but poses a threat to the environment and health. Chronic exposure to DLM may cause kidney injury, primarily through inducing apoptosis and fibrosis via inhibition of the Nrf2/p38MAPK pathway.