Maresin-1通过ALX/NF-κB通路促进巨噬细胞的自噬

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Abstract Objective: To detect the activation of macrophage autophgy caused by maresin-1 (MaR1) and the possible related signaling pathway. Methods: The mice bone marrow-derived macrophages (BMDMs) was cultured in vitro. The expressin of LC3B was observed under laser scanning confocal microscope, the ratio of LC3B and LC3A was detected by Western blot, the expresion of ATG5, ATG7, BECN-1 gene were detected by qPCR after giving MaR1. Then macrophages were pretreated separately with lysosomal inhibitors (CQ), PI3K inhibitors (LY294002), mTOR inhibitors (rapamycin), ALX inhibitors (Boc-2), and the ratio of LC3B and LC3A or the expression of beclin-1 were detected. Results: Mice BMDMs were consisted of approximately 90% F4/80 expression asassessed by flow cytometry. The expression of LC3B was distinctly increased when given MaR1 which observed under laser scanning confocal microscope (P<0.05), so is the ratio of LC3B and LC3A which detected by Western blot (P<0.05), and the expression of ATG5, ATG7, BECN-1 which detected by qPCR (P<0.01). When cells were pretreated by CQ or rapamycin, the effect of MaR1 was not diappeared, when pretreated by LY294002, the effect of MaR1 was diappeared. After treatment by MaR1, the expression of p50 was increased (P<0.01), the effect of MaR1 in the macropages come from p50 KO mice was disappeard. Conclusion: MaR1 activates autophagy in macrophages via ALX/NF-κB pathway.

Key words： autophagy maresin-1 NF-kappa B macrophages mTOR

Received: 01 March 2017

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	LIN Jing
	LUO Lingchun
	CAO Bingbing
	JIN Shengwei
	GAO Fang.

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2017/V47/I7/474

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