Tanreqing Injection Inhibits Activation of NLRP3 Inflammasome in Macrophages Infected with Influenza A Virus by Promoting Mitophagy.
10.1007/s11655-024-3905-3
- Author:
Tian-Yi LIU
1
;
Yu HAO
1
;
Qin MAO
1
;
Na ZHOU
1
;
Meng-Hua LIU
1
;
Jun WU
1
;
Yi WANG
2
;
Ming-Rui YANG
3
,
4
Author Information
1. School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 102488, China.
2. Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
3. School of Life Sciences, Beijing University of Chinese Medicine, Beijing, 102488, China. mingruiyang@
4. com.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
Tanreqing Injection;
anti-inflammation;
influenza virus;
mitophagy;
nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 inflammasome
- MeSH:
Mitophagy/drug effects*;
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism*;
Animals;
Macrophages/virology*;
Inflammasomes/drug effects*;
Drugs, Chinese Herbal/pharmacology*;
Mice;
Mitochondria/metabolism*;
Reactive Oxygen Species/metabolism*;
Influenza A virus/physiology*;
Interleukin-1beta/metabolism*;
Cell Line;
Injections
- From:
Chinese journal of integrative medicine
2025;31(1):19-27
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the inhibitory effect of Tanreqing Injection (TRQ) on the activation of nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome in macrophages infected with influenza A virus and the underlying mechanism based on mitophagy pathway.
METHODS:The inflammatory model of murine macrophage J774A.1 induced by influenza A virus [strain A/Puerto Rico/8/1934 (H1N1), PR8] was constructed and treated by TRQ, while the mitochondria-targeted antioxidant Mito-TEMPO and autophagy specific inhibitor 3-methyladenine (3-MA) were used as controls to intensively study the anti-inflammatory mechanism of TRQ based on mitophagy-mitochondrial reactive oxygen species (mtROS)-NLRP3 inflammasome pathway. The levels of NLRP3, Caspase-1 p20, microtubule-associated protein 1 light chain 3 II (LC3II) and P62 proteins were measured by Western blot. The release of interleukin-1β (IL-1β) was tested by enzyme linked immunosorbent assay, the mtROS level was detected by flow cytometry, and the immunofluorescence and co-localization of LC3 and mitochondria were observed under confocal laser scanning microscopy.
RESULTS:Similar to the effect of Mito-TEMPO and contrary to the results of 3-MA treatment, TRQ could significantly reduce the expressions of NLRP3, Caspase-1 p20, and autophagy adaptor P62, promote the expression of autophagy marker LC3II, enhance the mitochondrial fluorescence intensity, and inhibit the release of mtROS and IL-1β (all P<0.01). Moreover, LC3 was co-localized with mitochondria, confirming the type of mitophagy.
CONCLUSION:TRQ could reduce the level of mtROS by promoting mitophagy in macrophages infected with influenza A virus, thus inhibiting the activation of NLRP3 inflammasome and the release of IL-1β, and attenuating the inflammatory response.
