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SIRT7 Regulates Lipopolysaccharide-Induced Inflammatory Injury by Suppressing the NF-kappa B Signaling Pathway

文献类型： 外文期刊

作者： Chen, Kun-Lin 1 ; Li, Lian 1 ; Li, Cheng-Min 1 ; Wang, Yi-Ru 1 ; Yang, Fang-Xiao 1 ; Kuang, Mei-Qian 1 ; Wang, Gen-Lin 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Jiangsu, Peoples R China

2.Jiangsu Acad Agr Sci, Inst Anim Sci, Nanjing 210014, Jiangsu, Peoples R China

期刊名称：OXIDATIVE MEDICINE AND CELLULAR LONGEVITY （ 影响因子：6.543； 五年影响因子：7.454 ）

ISSN： 1942-0900

年卷期： 2019 年

页码：

收录情况： SCI

摘要： Mastitis has severely affected the cattle industry worldwide and has resulted in decreased dairy production and cattle reproduction. Although prevention and treatment methods have been implemented for decades, cattle mastitis is still an intractable disease. Sirtuin 7 (SIRT7) is an NAD(+)-dependent deacetylase that is involved in various biological processes, including ribosomal RNA synthesis and protein synthesis, DNA damage response, metabolism, and tumorigenesis. However, whether SIRT7 participates in inflammation remains unknown. Our results revealed that SIRT7 is downregulated in tissue samples from mastitic cattle. Therefore, we isolated dairy cow mammary epithelial cells (DCMECs) from breast tissues and developed an in vitro model of lipopolysaccharide- (LPS-) induced inflammation to examine SIRT7 function and its potential role in inflammation. We showed that SIRT7 was significantly downregulated in LPS-treated DCMECs. SIRT7 knockdown significantly increased the LPS-stimulated production of inflammatory mediators, like reactive oxygen and nitric oxide, and upregulated TAB1 and TLR4. In addition, SIRT7 knockdown significantly increased the phosphorylation of TAK1 and NF-kappa Bp65 in LPS-treated DCMECs. Moreover, SIRT7 knockdown promoted the translocation of NF-kappa Bp-p65 to the cell nucleus and then increased the secretion of inflammatory cytokines (IL-1 and IL-6). In contrast, SIRT7 overexpression had the opposite effects when compared to SIRT7 knockdown in LPS-treated DCMECs. In addition, SIRT7 overexpression attenuated LPS-induced DCMEC apoptosis. Taken together, our results indicate that SIRT7 can suppress LPS-induced inflammation and apoptosis via the NF-kappa B signaling pathway. Therefore, SIRT7 may be considered as a potential pharmacological target for clinical mastitis therapy.

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