Journal of ethnopharmacology · 2026
Platycodin D restricts NDV replication via modulation of MAPK, NLRP3 inflammasome and interferon signaling.
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Gao Pei, Peng Bosen, Ding Jianlei, Chen Libin, Fan Lei, Li Xinshan, Jin Shangwei, Yang Sen, Liu Fei, Yang Jiayun, Iqbal Munir, Munir Muhammad, Chao Limin, Liu Zhike, Wang Mengdong, Ren Tao, Ma Jinyou
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Platycodon grandiflorus (PG) is a traditional herb widely used for respiratory infections. Newcastle disease virus (NDV) is a highly contagious and devastating pathogen that causes severe economic losses to the poultry industry. Platycodin D (PD), a bioactive component of PG, has not been investigated for its antiviral activity against NDV.
AIM OF THE STUDY: We investigated the antiviral activity of PD against NDV and elucidated its underlying host-targeted mechanisms.
MATERIALS AND METHODS: The anti-NDV activity of PD was evaluated in vitro and in vivo. Transcriptomic and network pharmacology were employed to map PD-targeted pathways. Mechanistic dissection was achieved by examining MAPK signaling cascade, NLRP3 inflammasome assembly, inflammatory cytokine profiling, apoptosis regulation, and type I interferon response.
RESULTS: PD significantly inhibited NDV replication in vitro and in vivo, reducing viral loads and tissue injury in infected chickens. Transcriptomic profiling combined with network pharmacology analysis identified inflammation-, apoptosis-, and interferon-related pathways as major targets of PD, with MAPK signaling emerging as a central regulatory node. Mechanistic studies demonstrated that PD suppressed NDV-induced activation of the MAPK pathway and NLRP3 inflammasome assembly, leading to decreased production of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and IL-18). In parallel, PD attenuated virus-induced apoptosis through upregulation of the anti-apoptotic protein Bcl-2. Moreover, PD enhanced antiviral immunity by promoting IFN-α/β expression and STAT1 phosphorylation.
CONCLUSION: PD restricts NDV infection by coordinately modulating host inflammatory, apoptotic, and innate antiviral signaling pathways, supporting its potential as a host-targeted antiviral candidate for the control of Newcastle disease.
AIM OF THE STUDY: We investigated the antiviral activity of PD against NDV and elucidated its underlying host-targeted mechanisms.
MATERIALS AND METHODS: The anti-NDV activity of PD was evaluated in vitro and in vivo. Transcriptomic and network pharmacology were employed to map PD-targeted pathways. Mechanistic dissection was achieved by examining MAPK signaling cascade, NLRP3 inflammasome assembly, inflammatory cytokine profiling, apoptosis regulation, and type I interferon response.
RESULTS: PD significantly inhibited NDV replication in vitro and in vivo, reducing viral loads and tissue injury in infected chickens. Transcriptomic profiling combined with network pharmacology analysis identified inflammation-, apoptosis-, and interferon-related pathways as major targets of PD, with MAPK signaling emerging as a central regulatory node. Mechanistic studies demonstrated that PD suppressed NDV-induced activation of the MAPK pathway and NLRP3 inflammasome assembly, leading to decreased production of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and IL-18). In parallel, PD attenuated virus-induced apoptosis through upregulation of the anti-apoptotic protein Bcl-2. Moreover, PD enhanced antiviral immunity by promoting IFN-α/β expression and STAT1 phosphorylation.
CONCLUSION: PD restricts NDV infection by coordinately modulating host inflammatory, apoptotic, and innate antiviral signaling pathways, supporting its potential as a host-targeted antiviral candidate for the control of Newcastle disease.