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J Immunol. 2017 Nov 15;199(10):3466-3477. doi: 10.4049/jimmunol.1602016. Epub 2017 Oct 9.

Naringenin Ameliorates Acute Inflammation by Regulating Intracellular Cytokine Degradation.

Author information

1
Protein and Peptide Pharmaceutical Laboratory, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; and.
2
Winship Cancer Institute of Emory University, Atlanta, GA 30322.
3
Protein and Peptide Pharmaceutical Laboratory, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; and weixx@sun5.ibp.ac.cn zhangcl@moon.ibp.ac.cn.

Abstract

Ungoverned activation of innate and adaptive immunity results in acute inflammatory disease, such as bacteria-induced endotoxemia and fulminant hepatitis by virus infection. Thus, therapeutic control of inflammation is crucial for clinical management of many human diseases. In murine models of LPS- and Con A-induced liver injury, we found that naringenin, a natural predominant flavanone, is capable of protecting against lethality induced by LPS and preventing inflammation-induced organ injury. The protective effect of naringenin is mediated by reducing the levels of several inflammatory cytokines. Unexpectedly, naringenin inhibits TNF-α and IL-6 secretion in macrophages and T cells without interfering with the TLR signaling cascade, cytokine mRNA stability, or protein translation. These results indicate the existence of a posttranslational control mechanism. Further studies show that naringenin enhances intracellular cytokine degradation through lysosome- and TFEB-dependent mechanisms. This study provides evidence that naringenin has the capacity to dampen cytokine production by regulating lysosome function. Thus, naringenin may represent a potential therapeutic agent for controlling inflammation-related diseases.

PMID:
28993518
DOI:
10.4049/jimmunol.1602016
[Indexed for MEDLINE]
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