Abstract: Acetochlor (ACT) is a widely used herbicide in agriculture and has become a global organic pollutant, posing significant environmental risks. As an aniline herbicide, ACT threatens kidney health through inflammatory responses. Omega-3 (Ω3) fatty acids play a crucial role in anti-inflammatory processes. This study investigates the protective effects of Ω3 against ACT-induced renal damage and the specific molecular mechanisms underlying these protective effects. Our findings indicate that exposure to ACT leads to renal inflammation and lipid-metabolism disorders, while Ω3 alleviates inflammation levels and improves lipid-metabolism abnormalities. Mechanistically, Ω3 mitigates the damage caused by ACT via the endoplasmic reticulum (ER) stress-NLRP3 inflammasome axis. Ω3 stabilizes the structure of GRP78, a key ER stress sensor, thereby preventing the activation of downstream pathways associated with ER stress, including the transcription factor CHOP. This stabilization subsequently reduces assembly of the downstream NLRP3 inflammasome complex, thereby alleviating kidney damage. These results provide new insights into the role of Ω3 in modulating ER stress and its anti-inflammatory mechanisms in an avian acetochlor-induced renal injury model.
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Open peer comments: Debate/Discuss/Question/Opinion
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