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Objective: To explore the effect of sinomenine （SIN） on LPS-induced apoptosis and autophagy of lung epithelial cells through the JNK/c-Jun signaling pathway. Methods: MLE-12 lung epithelial cells were cultured, and the toxicity of SIN was detected by CCK-8. Apoptosis was detected by flow cytometry, the number of autophagosomes was detected by immunofluorescence, and the expression levels of apoptosis, autophagy and JNK/c-Jun signaling pathway-related proteins were detected by Western blot. Results: After LPS modeling, apoptosis rate and the number of autophagosomes were increased, the protein levels of Cleaved caspase-3, Bax, and Beclin-1, and LC3Ⅱ/LC3Ⅰ, p-JNK/JNK and p-c-Jun/c-Jun were increased （P<0.05）; Bcl-2 and P62 protein levels were decreased （P<0.05）. SIN treatment can significantly improve the effects of LPS on apoptosis and autophagy, as well as the regulation of the JNK/c-Jun signaling pathway （P<0.05）. Treatment with the autophagy inhibitor 3-MA or the JNK agonist ANISO could partially reverse the protective effect of SIN on LPS-induced lung epithelial cells （P<0.05）. Conclusion: SIN may increase autophagy and protect lung epithelial cells damaged by LPS by regulating proteins related to the JNK/c-Jun signaling pathway. [ABSTRACT FROM AUTHOR]

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