Journal of ethnopharmacology · 2026
Mechanistic investigation of modified Ma-Xing-Shi-Gan Decoction in the treatment of Klebsiella pneumoniae pneumonia via the V-ATPase/ATG16L1 pathway.
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Jiang Qirui, Geng Ruizhi, Sun Xiaoluo, Tao Sian, Liu Haihui, Zhang Jing, Liang Yu, Wu Wenjun, Liu Wenping, Xi Chongcheng, Wang Dong, Mao Yi, Li Baixue, Feng Quansheng, Liu Jibin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Modified Ma-Xing-Shi-Gan Decoction (MMXSGD) has been widely used in the treatment of Klebsiella pneumoniae (KP)-induced pneumonia, which is derived from the classical traditional Chinese medicine formula Ma-Xing-Shi-Gan Decoction.
AIM OF THE STUDY: This study aimed to investigate the therapeutic effects of MMXSGD on KP-induced pneumonia and to elucidate whether its protective effects are mediated through activation of the V-ATPase/ATG16L1-dependent xenophagy pathway and regulation of macrophage polarization.
MATERIALS AND METHODS: A mouse model of KP-induced pneumonia was established via tracheal incubation. The therapeutic efficacy of MMXSGD was assessed by survival rate, lung index, and pulmonary function parameters. Subsequently, lung inflammatory injury, hematological changes, cytokine levels, and the formation of xenophagosomes and xenophagolysosomes were evaluated using H&E staining, routine blood tests, ELISA, immunofluorescence, and transmission electron microscopy (TEM). The gene and protein expression levels of the V-ATPase-ATG16L1 xenophagy pathway after MMXSGD treatment were measured by RT-qPCR and western blotting.
RESULTS: Compared with the model group, MMXSGD treatment increased the 5-day survival rate by approximately 50% and markedly attenuated pathological lung injury. The levels of TNF-α, IL-6, and IL-1β in serum and BALF were significantly lower in the MMXSGD group than in the model group (p < 0.05). Immunofluorescence analysis revealed that MMXSGD treatment markedly reduced KP-positive cells, improved cellular morphology, and significantly increased xenophagosomes and xenophagolysosomes formation. Furthermore, MMXSGD significantly up-regulated the gene expression of ATP6V0C, ATG16L1, and Map1lc3b in the xenophagy pathway (p < 0.05). It also increased V-ATPase, ATG16L1, and LC3B expression. LC3B showed a clear shift from the cytosolic LC3-I form to the membrane-associated LC3-II form, indicating enhanced xenophagy. In addition, LC3B showed a clear shift from the cytosolic LC3-I form to the membrane-associated LC3-II form, indicating enhanced xenophagy.
CONCLUSION: These findings suggest that MMXSGD mitigates inflammatory injury in KP-induced pneumonia by modulating macrophage polarization through the activation of the V-ATPase-ATG16L1-mediated xenophagy pathway.
AIM OF THE STUDY: This study aimed to investigate the therapeutic effects of MMXSGD on KP-induced pneumonia and to elucidate whether its protective effects are mediated through activation of the V-ATPase/ATG16L1-dependent xenophagy pathway and regulation of macrophage polarization.
MATERIALS AND METHODS: A mouse model of KP-induced pneumonia was established via tracheal incubation. The therapeutic efficacy of MMXSGD was assessed by survival rate, lung index, and pulmonary function parameters. Subsequently, lung inflammatory injury, hematological changes, cytokine levels, and the formation of xenophagosomes and xenophagolysosomes were evaluated using H&E staining, routine blood tests, ELISA, immunofluorescence, and transmission electron microscopy (TEM). The gene and protein expression levels of the V-ATPase-ATG16L1 xenophagy pathway after MMXSGD treatment were measured by RT-qPCR and western blotting.
RESULTS: Compared with the model group, MMXSGD treatment increased the 5-day survival rate by approximately 50% and markedly attenuated pathological lung injury. The levels of TNF-α, IL-6, and IL-1β in serum and BALF were significantly lower in the MMXSGD group than in the model group (p < 0.05). Immunofluorescence analysis revealed that MMXSGD treatment markedly reduced KP-positive cells, improved cellular morphology, and significantly increased xenophagosomes and xenophagolysosomes formation. Furthermore, MMXSGD significantly up-regulated the gene expression of ATP6V0C, ATG16L1, and Map1lc3b in the xenophagy pathway (p < 0.05). It also increased V-ATPase, ATG16L1, and LC3B expression. LC3B showed a clear shift from the cytosolic LC3-I form to the membrane-associated LC3-II form, indicating enhanced xenophagy. In addition, LC3B showed a clear shift from the cytosolic LC3-I form to the membrane-associated LC3-II form, indicating enhanced xenophagy.
CONCLUSION: These findings suggest that MMXSGD mitigates inflammatory injury in KP-induced pneumonia by modulating macrophage polarization through the activation of the V-ATPase-ATG16L1-mediated xenophagy pathway.