Chinese journal of integrative medicine · 2026
Maxing Shigan Decoction Regulates Immune Inflammatory Response of Adenovirus Pneumonia by Inhibiting cGAS-STING Pathway.
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Wang Si-Wei, Peng Cheng, Deng Li, Cong Guo-Qian, Yan Feng, Na Jun-Fu, Pang Li-Jian
Аннотация
OBJECTIVE: To investigate whether Maxing Shigan Decoction (MSD) regulates the immune-inflammatory response of adenovirus pneumonia (AVP) by inhibiting the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway.
METHODS: A mouse model of AVP was induced by intranasal instillation of human adenovirus type 3 (Ad3), and Raw264.7 cells were infected with Ad3 to establish an in vitro model. The in vivo and in vitro experiments both included 6 groups: control, model, ribavirin (RIB), and low- (MSD-L), medium- (MSD-M), and high-dose MSD (MSD-H) groups. Moreover, the cGAS-STING pathway agonist SR-717 was used during the cell experiment. Hematoxylin and eosin (HE) staining was conducted to identify pathological changes in the lung tissue of AVP mice. The quantity of CD3+CD8+ T cells in the mouse lung tissue was evaluated using flow cytometry. The expression levels of cGAS, STING, interferon-β (IFN-β), TANK binding kinase 1 (TBK1), and interferon regulatory factor 3 (IRF3) were assessed by Western blot for protein levels and quantitative polymerase chain reaction for mRNA levels.
RESULTS: In vivo, MSD and RIB significantly reduced lung tissue inflammation in the AVP mouse model, and reduced the excessive immune response mediated by CD3+CD8+ T cells (P<0.01). The cGAS, STING, IFN-β, TBK1, and IRF3 protein and mRNA levels were markedly elevated in model mice (P<0.01), while treatment with MSD and RIB significantly reduced these levels (P<0.01). In vitro experiments showed the similar results of levels of cGAS, STING, IRF3, TBK1, and IFN-β proteins and mRNAs. However, these levels significantly decreased with MSD and RIB treatment were restored after treatment with SR-717 (P<0.01).
CONCLUSIONS: MSD modulated the immune inflammatory response in AVP by inhibiting the cGAS-STING pathway. It protected lung tissue from damage caused by excessive immune responses and inflammatory reactions.
METHODS: A mouse model of AVP was induced by intranasal instillation of human adenovirus type 3 (Ad3), and Raw264.7 cells were infected with Ad3 to establish an in vitro model. The in vivo and in vitro experiments both included 6 groups: control, model, ribavirin (RIB), and low- (MSD-L), medium- (MSD-M), and high-dose MSD (MSD-H) groups. Moreover, the cGAS-STING pathway agonist SR-717 was used during the cell experiment. Hematoxylin and eosin (HE) staining was conducted to identify pathological changes in the lung tissue of AVP mice. The quantity of CD3+CD8+ T cells in the mouse lung tissue was evaluated using flow cytometry. The expression levels of cGAS, STING, interferon-β (IFN-β), TANK binding kinase 1 (TBK1), and interferon regulatory factor 3 (IRF3) were assessed by Western blot for protein levels and quantitative polymerase chain reaction for mRNA levels.
RESULTS: In vivo, MSD and RIB significantly reduced lung tissue inflammation in the AVP mouse model, and reduced the excessive immune response mediated by CD3+CD8+ T cells (P<0.01). The cGAS, STING, IFN-β, TBK1, and IRF3 protein and mRNA levels were markedly elevated in model mice (P<0.01), while treatment with MSD and RIB significantly reduced these levels (P<0.01). In vitro experiments showed the similar results of levels of cGAS, STING, IRF3, TBK1, and IFN-β proteins and mRNAs. However, these levels significantly decreased with MSD and RIB treatment were restored after treatment with SR-717 (P<0.01).
CONCLUSIONS: MSD modulated the immune inflammatory response in AVP by inhibiting the cGAS-STING pathway. It protected lung tissue from damage caused by excessive immune responses and inflammatory reactions.