Abstract: 【Objective】 To detect the role of P38/MAPK signaling pathways in the activation of autophagy in macrophages caused by lipopolysaccharide. 【Methods】 The macrophage cell line RAW264.7 cultured in vitro

and was divided into five groups according culture environment

including normal culture group

starvation activates autophagy group

simple LPS group

LPS+P38 inhibitor (SB203582) group and LPS+mTOR inhibitors (rapamycin) group. Fluorescent expression vector pcDNA3.1-GFP-LC3 constructed in previous work

was transfected into macrophages

and the fluorescence microscopy was used to detect the autophagosome formation in each group. qRT-PCR was used to detect autophagy associated genes Atg5

Atg7

LC3-Ⅱ and Bnip3 expression levels in each group. Western Blot was used to test LC3-Ⅱ

p-P38

P38 expression in each group

so as to evaluate LPS activated macrophages autophagy molecular pathways. 【Results】 We successfully got the stably expressing GFP-LC3 macrophages

which can be used to observe the autophagy under a fluorescence microscope. The autophages in starvation group

LPS stimulation+SB203582 group and LPS stimulation+ rapamycin group were significantly increased. qRT-PCR detected that autophagy-related genes Atg5

Atg7

LC3-Ⅱ and Bnip3 expression levels were significantly increased in starvation group

LPS stimulation+SB203582 group and LPS stimulation+rapamycin group. Western Blot showed that p-P38 in starvation group

LPS group and LPS stimulation+rapamycin group was significantly increased. LC3-Ⅱexpression level in starvation group

LPS stimulation+SB203582 group and LPS stimulation+rapamycin was higher than control group and LPS group. 【Conclusions】 LPS can regulate macrophage autophagy

and p38/MAPK pathway is one of its down-regulated pathways besides the classic PI3K/Akt/mTOR pathway.