Mycoplasma pneumoniae (MP) is one of the main pathogens causing community acquired pneumonia (CAP) in children and adults. Previous pharmacological and clinical studies have shown that Polydatin (PD) exerts anti-inflammatory action by conferring protective benefit in MP pneumonia. However, the mechanism underlying the of PD on MP infection remains unclear. It was found that PD alleviated MP-induced injury by inhibiting caspase-1/gasdermin D (GSDMD)-mediated epithelial pyroptosis. The results demonstrated that PD inhibited the transformation of GSDMD to N-terminal gasdermin-N (GSDMD-N) by decreasing caspase-1 activation, as well as suppressed the formation and secretion of interleukin-1β (IL-1β) and interleukin-18 (IL-18), reversed Na, K-ATPase reduction, and suppressed LDH release both in vitro and vivo. Taken together, epithelial pyroptosis in BEAS‐2B cells and lung injury in mice were prevented by PD. In conclusion, PD suppressed pulmonary injury triggered by MP infection, by inhibiting the caspase-1/GSDMD-mediated epithelial pyroptosis signaling pathway. Thus, PD may be regarded as a potential therapy for MP-induced inflammation.

肺炎支原体（MP）是引起儿童和成人社区获得性肺炎（CAP）的主要病原体之一。先前的药理学和临床研究表明，虎杖甙 (PD) 通过赋予 MP 肺炎保护作用而发挥抗炎作用。然而，PD对MP感染的作用机制仍不清楚。研究发现，PD 通过抑制 caspase-1/gasdermin D (GSDMD) 介导的上皮细胞焦亡来减轻 MP 引起的损伤。结果表明，PD通过减少caspase-1的激活来抑制GSDMD向N端gasdermin-N（GSDMD-N）的转化，并抑制白细胞介素1β（IL-1β）和白细胞介素18的形成和分泌。 (IL-18)，逆转 Na、K-ATP 酶的减少，并在体外和体内抑制 LDH 释放。综上所述，PD 可以预防 BEAS-2B 细胞的上皮焦亡和小鼠的肺损伤。总之，PD 通过抑制 caspase-1/GSDMD 介导的上皮细胞焦亡信号通路，抑制 MP 感染引发的肺损伤。因此，PD 可能被视为治疗 MP 引起的炎症的潜在疗法。