Dehydroepiandrosterone attenuates LPS-induced inflammatory responses via activation of Nrf2 in RAW264.7 macrophages
文献类型： 外文期刊
作者： Cao, Ji 1 ; Li, Qian 1 ; Shen, Xuehuai 3 ; Yao, Yao 1 ; Li, Longlong 1 ; Ma, Haitian 1 ;
作者机构： 1.Nanjing Agr Univ, Coll Vet Med, Key Lab Anim Physiol & Biochem, Nanjing 210095, Peoples R China
2.Nanjing Agr Univ, Coll Vet Med, MOE Joint Int Res Lab Anim Hlth & Food Safety, Nanjing 210095, Peoples R China
3.Anhui Acad Agr Sci, Inst Anim Husb & Vet Sci, Livestock & Poultry Epidem Dis Res Ctr Anhui Prov, Hefei 230001, Peoples R China
关键词： Dehydroepiandrosterone; Lipopolysaccharide; Inflammation; Nrf2; NF-kappa B
期刊名称：MOLECULAR IMMUNOLOGY （ 影响因子：4.407； 五年影响因子：4.227 ）
ISSN： 0161-5890
年卷期： 2021 年 131 卷
页码：
收录情况： SCI
摘要： Dehydroepiandrosterone (DHEA) is the major steroid hormone in humans and animals, which can regulate the body's inflammatory responses. However, the detail mechanism of this beneficial function is still poorly understood. The present study aimed to explore the anti-inflammation effect of DHEA and its underlying molecular mechanism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The findings showed that DHEA significantly inhibited the inflammation-related mediators production and pro-inflammatory cytokines expression level. Further research found that DHEA obviously blocked the LPS-stimulated PI3K/AKT, MAPK and NF-kappa B activation in RAW 264.7 cells. Meanwhile, DHEA enhanced the autophagy-dependent Keap1 protein degradation, subsequently activated the Nrf2 pathway to alleviate the redox imbalance and inflammatory responses. In conclusion, our data demonstrated that DHEA suppresses inflammatory responses through the activation of Nrf2 and inhibition of NF-kappa B in LPS-stimulated macrophages.
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