Bifidobacterium lactis BB-12 Attenuates Macrophage Aging Induced by D-Galactose and Promotes M2 Macrophage Polarization

被引:15
作者
Zhang, Da-yong [1 ]
Pan, Zheng-yang [1 ]
Yu, Xiong-kai [1 ]
Chen, Yi-fan [1 ]
Gao, Chen-hao [1 ]
Yang, Yu-tian [1 ]
Jiang, Xue-fan [2 ,3 ]
Li, Na [1 ]
Pan, Jian-ping [1 ]
机构
[1] Zhejiang Univ City Coll, Sch Med, Dept Clin Med, Hangzhou 310015, Peoples R China
[2] Zhejiang Prov Peoples Hosp, Dept Otorhinolaryngol, Hangzhou 310014, Zhejiang, Peoples R China
[3] Hangzhou Med Coll, Peoples Hosp, Hangzhou 310014, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
ACTIVATION; AGE; P16(INK4A); INFLAMMATION; SUPERNATANT; COMPONENTS; CULTURE; YOGURT; CELLS;
D O I
10.1155/2019/4657928
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Immunosenescence comprises a set of dynamic changes occurring in innate and adaptive immune systems, and macrophage aging plays an important role in innate and adaptive immunosenescence. However, function and polarization changes in aging macrophages have not been fully evaluated, and no effective method for delaying macrophage senescence is currently available. The results of this study reveal that D-galactose (D-gal) can promote J774A.1 macrophage senescence and induce macrophage M1 polarization differentiation. Bifidobacterium lactis BB-12 can significantly inhibit J774A.1 macrophage senescence induced by D-gal. IL-6 and IL-12 levels in the BB-12 groups remarkably decreased compared with that in the D-gal group, and the M2 marker, IL-10, and Arg-1 mRNA levels increased in the BB-12 group. BB-12 inhibited the expression of p-signal transducer and activator of transcription 1 (STAT1) and promoted p-STAT6 expression. In summary, the present study indicates that BB-12 can attenuate the J774A.1 macrophage senescence and induce M2 macrophage polarization, thereby indicating the potential of BB-12 to slow down immunosenescence and inflamm-aging.
引用
收藏
页数:12
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