Effects and mechanism of methionine restriction on macrophage for lipopolysaccharide-induced acute lung injury in mice
10.16016/j.2097-0927.202308112
- VernacularTitle:甲硫氨酸摄入限制对LPS诱导急性肺损伤小鼠巨噬细胞的影响及作用机制
- Author:
Xianjian LIAO
1
;
Jing WEN
;
Jiaxiang DUAN
;
Lunli XIANG
;
Zhen YANG
;
Qingying HE
;
Jiaolin NING
Author Information
1. 400038 重庆,陆军军医大学(第三军医大学)第一附属医院麻醉科
- Keywords:
acute lung injury;
macrophage;
methionine restriction;
chemokines;
lipopolysaccharide
- From:
Journal of Army Medical University
2024;46(7):688-694
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of methionine restriction(MR)on macrophages in lipopolysaccharide(LPS)-induced acute lung injury(ALI)and to explore the underlying mechanism.Methods According to the random number table method,36 male C57BL/6J mice(6～8 weeks old,23±2 g)were divided into 3 groups with 12 mice in each group:the sham group,the LPS group and the LPS+MR group.HE staining and pathological scoring of lung injury were performed in lung tissues.The expression of LPS-binding protein(LBP)and Toll-like receptor-4(TLR4)was detected by RT-qPCR and Western blotting.Macrophage-colony stimulating factor(M-CSF),granulocyte-macrophage-colony stimulating factor(GM-CSF)and chemokine C-C motif ligand 3(CCL3)which are all macrophage-associated chemokines were analyzed by immunohistochemistry.Results Compared with the sham group,the pathological score of lung injury in the LPS group was significantly increased(P＜0.01);The mRNA and protein expression levels of LBP and TLR4 were significantly increased;The number of positive cells of CD11b,F4/80,M-CSF,GM-CSF and CCL3 were significantly increased(P＜0.01).MR significantly improved LPS-induced ALI,and decreased the pathological score of lung injury(P＜0.01);The mRNA and protein expression levels of LBP and TLR4 were decreased;Compared with the LPS group,the number of positive cells of CD11 b,F4/80,M-CSF,GM-CSF and CCL3 were reduced in the LPS+MR group(P＜0.01).Conclusion MR could attenuate LPS-induced ALI by inhibiting the expression of macrophage chemokines and preventing infiltration and activation of macrophage to lungs.
