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cs.AI, q-bio.NC updates on arXiv.org
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6GAgentGym: Tool Use, Data Synthesis, and Agentic Learning for Network Management
arXiv:2603.29656v1 Announce Type: cross Abstract: Autonomous 6G network management requires agents that can execute tools, observe the resulting state changes, and adapt their decisions accordingly. Existing benchmarks based on static questions or scripted episode replay, however, do not support such closed-loop interaction, limiting agents to passive evaluation without the ability to learn from environmental feedback. This paper presents 6GAgentGym to provide closed-loop capability. The framew
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Omics In Lung
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Dunhuang Daxiefei Decoction ameliorates acute lung injury via the HIF-1alpha/glycolysis/H3K18la axis
J Ethnopharmacol. 2026 Mar 26;365:121591. doi: 10.1016/j.jep.2026.121591. Online ahead of print.ABSTRACTETHNOPHARMACOLOGICAL RELEVANCE: Acute lung injury (ALI) lacks effective therapies. HIF-1Ξ±-driven glycolysis can promote histone lactylation and sustain pro-inflammatory (M1) macrophage responses. Daxiefei Decoction (DXFD), a classic traditional Chinese medicine formula, is used for pulmonary inflammatory diseases, but its immunometabolic mechanism remains unclear.AIM OF THE STUDY: To evaluate
Dunhuang Daxiefei Decoction ameliorates acute lung injury via the HIF-1alpha/glycolysis/H3K18la axis
J Ethnopharmacol. 2026 Mar 26;365:121591. doi: 10.1016/j.jep.2026.121591. Online ahead of print.
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE: Acute lung injury (ALI) lacks effective therapies. HIF-1Ξ±-driven glycolysis can promote histone lactylation and sustain pro-inflammatory (M1) macrophage responses. Daxiefei Decoction (DXFD), a classic traditional Chinese medicine formula, is used for pulmonary inflammatory diseases, but its immunometabolic mechanism remains unclear.
AIM OF THE STUDY: To evaluate the protective efficacy of DXFD against lipopolysaccharide (LPS)-induced ALI and to determine whether it acts through the HIF-1Ξ±/glycolysis/histone H3K18 lactylation (H3K18la) axis to regulate macrophage polarization.
MATERIALS & METHODS: DXFD constituents were characterized by UPLC-LTQ-Orbitrap-MS/MS, followed by network pharmacology, molecular docking, and molecular dynamics (MD) simulations. Lung transcriptomics and metabolomics were performed in ALI mice. Efficacy and mechanisms were assessed in LPS-challenged mice and RAW264.7 macrophages using histopathology, ELISA, qRT-PCR, Western blotting, and immunofluorescence. HIF-1Ξ± overexpression was used for validation.
RESULTS: DXFD dose-dependently alleviated lung injury and reduced pro-inflammatory cytokines in vivo, and suppressed M1 polarization in vivo and in LPS-stimulated macrophages. Multi-omics indicated activation of HIF-1Ξ±-associated inflammatory and glycolytic programs in ALI, which were normalized by DXFD. DXFD decreased glycolytic enzyme expression and reduced histone H3K18 lactylation (H3K18la); these effects were partially reversed by HIF-1Ξ± overexpression. Molecular docking and dynamics suggested stable binding of baicalin to HIF-1Ξ±.
CONCLUSIONS: DXFD mitigates ALI by dampening HIF-1Ξ±-dependent glycolysis and H3K18la, thereby restraining M1-driven inflammatory amplification.
PMID:41903585 | DOI:10.1016/j.jep.2026.121591