ArticleFrontiers in cell and developmental biology2026
Mechanistic and clinical investigation of Jiajiang Xuming decoction in multi-modal programmed cell death in stroke-associated pneumonia.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Stroke-Associated Pneumonia (SAP) is one of the leading causes of sepsis and ICU mortality among stroke patients, attributed to dysregulated immune responses as well as multiple MODES of cell death. Jiajiang Xuming Decoction (JXD) is a traditional Chinese medicine (TCM) formula to treat the symptoms of Wind-Phlegm-Stasis Obstruction Syndrome, blamed for all SAP-related sepsis. Methods: A single-centre retrospective cohort study was conducted in 100 ICU patients with microbiologically confirmed sepsis (Sepsis-3 criteria): 58 Stroke-Associated Pneumonia (SAP) and 42 non-SAP sepsis, compared to thirty healthy controls. On admission, Day 3 and Day 7, serial inflammatory markers (IL-6, IL-1β, TNF-α PCT CRP) and organ-function indicators were measured (hepatic: ALT AST; renal: creatinine (BUN); cardiac: cTnI† NT-proBNP). Therapeutic efficacy of JXD was evaluated in a propensity-score-matched (JXD n = 29; conventional treatment n = 29) sub-cohort. Mechanistic evidence were derived from scRNA-seq and an Results: Compared to non-SAP sepsis, SAP patients had significantly higher levels of inflammatory cytokines, markers of hepatic injury (ALT, AST), renal impairment (creatinine, BUN), and cardiac injury (cTnI, NT-proBNP) all P < 0.001; FDR q < 0.001). An AUC = 0.872 for SAP diagnosis with a combination of four markers (PCT + IL-6 + ALT + creatinine) was established. Supplemental JXD therapy provided a significant advantage over conventional treatment in Day-7 clinical improvement rate (72.4% vs. 48.3%, P = 0.048) and shortened ICU stay (12.1 vs. 16.3 days, P = 0.002), along with markers of mode microbiome-related inflammation and injury reduction in this population of patients with acute disturbances post-septic organs (Galluzzi et al., Cell Death Differ, 2018, 25(3), 486-541). JXD basically inhibited apoptosis (CASP3), pyroptosis (NLRP3), necroptosis (RIPK3) Conclusion: Multi-organ dysfunction biomarkers independently predicts sepsis sequelae post-SAP (AUC = 0.872)) and track treatments response Conclusions: JXD modulates a number of cellular death pathways
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