降植烷通过内质网应激诱导大鼠巨噬细胞自噬

Objective: To investigate the mechanism of pristane inducing autophagy in macrophages. Methods: Pristane was used to stimulate NR8383, a rat macrophage cell line. The changes in signaling pathways of AMPK, mTOR, and endoplasmic reticulum(ER)stress pathways including eIF2α and IRE1α in the cell model, as well as the expression of transcriptional factor TFEB and its translocation to the nucleus, were detected by using Western blotting. ER stress pathways were intervened by using an inducer DTT or an inhibitor 4-PBA to determin its effect on mTOR expression and autophay. Results: In pristane-stimulated NR8383 cell model, ER stress pathway eIF2α was activated at 0.5 h after stimulation, and then mTOR expression was decreased at 1 and 3 h after stimulation. There was no change for AMPK and IRE1α pathways. With 4-PBA treatment, pristane-reduced mTOR expression and increased LC3-II were reversed, while with DTT treatment, mTOR expression decreased and LC3-II expression increased even more. Pristane induced the expression and activation of TFEB in NR8383 cells. Conclusion: Pristane induces ER stress and leads to autophagy enhancement in rat macrophages.