Journal of ethnopharmacology · 2025
Huopu Xialing decoction mitigates influenza A-induced pulmonary injury by inhibiting METTL3-Nlrp3(m6A) mediated NLRP3 inflammasome activation.
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Ou Guosen, Liu Tangjuan, Wu Sizhi, Wang Hao, Wang Shiqi, Wu Jialin, Chen Yaokang, Deng Li, Xu Lu, Xu Huachong, Chen Xiaoyin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Huopu Xialing Decoction (HXD) is a traditional Chinese medicine (TCM) formula widely used in the clinical treatment of respiratory viral infections. Despite its established application, the pharmacological mechanisms underlying its therapeutic effects against influenza remain to be fully elucidated.
AIM OF THE STUDY: This study aimed to investigate the protective effects of HXD against influenza A virus-induced lung inflammation and to explore the role of gut microbiota and epigenetic regulation in mediating these effects.
MATERIALS AND METHODS: An intranasal FM1 influenza virus infection model was established in mice. Lung histopathology was assessed by HE staining, and interleukin-1β (IL-1β) levels were measured using ELISA. Global N6-methyladenosine (m6A) methylation in lung tissues was detected by dot blot. RNA sequencing and SELECT™-m6A-qPCR were employed to identify and validate METTL3-mediated m6A modifications. 16S rRNA sequencing was used to profile gut microbiota alterations, and fecal microbiota transplantation (FMT) experiments were conducted to evaluate the role of microbiota in HXD-mediated effects.
RESULTS: HXD treatment significantly alleviated influenza-induced lung injury, suppressed IL-1β expression, and reduced METTL3-dependent m6A methylation of Nlrp3 mRNA. This was associated with decreased expression of NLRP3 inflammasome components, including ASC, pro-Caspase-1, cleaved-Caspase-1, GSDMD-N, and IL-1β. Furthermore, HXD modulated gut microbiota composition, marked by increased abundance of Lactobacillus and reduced Staphylococcus, which contributed to the downregulation of the pulmonary METTL3-Nlrp3 (m6A) axis.
CONCLUSION: HXD attenuates influenza-induced pulmonary inflammation by modulating the gut-lung axis and inhibiting METTL3-mediated m6A modification of Nlrp3, leading to suppression of NLRP3 inflammasome activation. These findings provide pharmacological evidence supporting the traditional use of HXD in respiratory infections and highlight the interplay between gut microbiota and epitranscriptomic regulation in the action of TCM.
AIM OF THE STUDY: This study aimed to investigate the protective effects of HXD against influenza A virus-induced lung inflammation and to explore the role of gut microbiota and epigenetic regulation in mediating these effects.
MATERIALS AND METHODS: An intranasal FM1 influenza virus infection model was established in mice. Lung histopathology was assessed by HE staining, and interleukin-1β (IL-1β) levels were measured using ELISA. Global N6-methyladenosine (m6A) methylation in lung tissues was detected by dot blot. RNA sequencing and SELECT™-m6A-qPCR were employed to identify and validate METTL3-mediated m6A modifications. 16S rRNA sequencing was used to profile gut microbiota alterations, and fecal microbiota transplantation (FMT) experiments were conducted to evaluate the role of microbiota in HXD-mediated effects.
RESULTS: HXD treatment significantly alleviated influenza-induced lung injury, suppressed IL-1β expression, and reduced METTL3-dependent m6A methylation of Nlrp3 mRNA. This was associated with decreased expression of NLRP3 inflammasome components, including ASC, pro-Caspase-1, cleaved-Caspase-1, GSDMD-N, and IL-1β. Furthermore, HXD modulated gut microbiota composition, marked by increased abundance of Lactobacillus and reduced Staphylococcus, which contributed to the downregulation of the pulmonary METTL3-Nlrp3 (m6A) axis.
CONCLUSION: HXD attenuates influenza-induced pulmonary inflammation by modulating the gut-lung axis and inhibiting METTL3-mediated m6A modification of Nlrp3, leading to suppression of NLRP3 inflammasome activation. These findings provide pharmacological evidence supporting the traditional use of HXD in respiratory infections and highlight the interplay between gut microbiota and epitranscriptomic regulation in the action of TCM.