Ginsenoside Re Inhibits NLRP3 Inflammasome Activation in Depressive Mice by Promoting PINK1-Mediated Mitophagy

被引:0
作者
Liu, Shan [1 ]
Zhang, Yue [2 ]
Zhou, Hao [2 ]
Ma, Yating [2 ]
Huang, Fangzhou [2 ]
Lei, Tianyuan [2 ]
Wang, Qingbin [2 ]
Yu, Shangmin [2 ]
机构
[1] Bengbu Med Univ, Sch Basic Med Sci, Dept Physiol, Bengbu 233000, Anhui, Peoples R China
[2] Bengbu Med Univ, Sch Pharm, Dept Pharmaceut, Bengbu 233000, Anhui, Peoples R China
关键词
ginsenoside Re; depression; PINK1; mitophagy; NLRP3; inflammasome; BEHAVIORS;
D O I
10.1021/acs.jafc.4c09773
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Ginsenoside Re (Re) was proved effective in improving depressive-like behaviors. However, the potential antidepressant mechanism of Re remains unrevealed. In this study, we investigated whether PINK1-mediated mitophagy and NLRP3 inflammasomes were linked to the antidepressant mechanism of Re in chronic unpredictable mild stress (CUMS) mice and lipopolysaccharide (LPS)-stimulated astrocytes. RNA sequencing and bioinformatics analyses were performed to discover the targets and pathways associated with Re. PTEN-induced putative kinase 1 (PINK1) knockdown was conducted to clarify the role of PINK1-mediated mitophagy in the antidepressant mechanism of Re. The outcomes showed that Re ameliorated depressive-like behaviors, activated PINK1-mediated mitophagy, and inhibited NLRP3 inflammasome activation. PINK1 knockdown attenuated the antidepressant effect of Re. The promotion of mitophagy and the decline of NLRP3 inflammasome activation caused by Re were reversed by PINK1 knockdown. In conclusion, Re inhibited NLRP3 inflammasome activation by promoting PINK1-mediated mitophagy to exert its antidepressant effect.
引用
收藏
页码:10934 / 10946
页数:13
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