Eucalyptol relieves imidacloprid-induced autophagy through the miR-451/Cab39/AMPK axis in Ctenopharyngodon idellus kidney cells†.

Abstract

Imidacloprid (IMI) is a widely used neonicotinoid insecticide that has toxic effects on nontarget organisms. 1,8-Cineole (eucalyptol) is purified from essential oils in several aromatic plants and can prevent xenobiotic toxicity. The kidney is a major organ for xenobiotic elimination and thus has high risk of exposure. The purpose of this research was to clarify the effect of IMI exposure on autophagy in fish kidney cells, determine the potential of eucalyptol to provide cytoprotection from the toxicity of the neonicotinoid pesticide IMI, and identify its mechanism of action. Therefore, the Ctenopharyngodon idellus kidney cell line (CIK cell) was treated with 20 mg/L IMI and/or 20 μM eucalyptol for 48 h as the research objective. The results showed that IMI exposure induced autophagy accompanied by advanced autophagy markers BNIP3, Beclin1 and LC3Ⅱ/Ⅰ in CIK cells, reduced the levels of miR-451, increased the expression of Cab39 and AMPK, inhibited AKT/mTOR signaling, and activated the JNK pathway. Eucalyptol treatment alleviated IMI-induced autophagy and relieved the activation of autophagy-associated signals. These results indicate that eucalyptol could alleviate IMI-induced autophagy through the miR-451/Cab39/AMPK axis in fish kidney cells. These results partly explained the mechanism of biological threat on fish under IMI exposure and the potential application value of EUC in aquaculture.