Objective: This study aims to investigate the therapeutic effects and underlying mechanisms of Xuanfei Baidu Decoction (XFBD) in a mouse model of dampness-heat toxin pneumonia. By exploring how XFBD exerts its effects, we seek to deepen our understanding of its role in treating pulmonary diseases and to address the current knowledge gap regarding its mechanisms of action, thereby supporting its clinical application. Methods: Ultra-high-performance liquid chromatography and high-resolution mass spectrometry (HRMS) were employed to analyze the chemical constituents of XFBD. The protective effects of XFBD were evaluated using a dampness-heat toxin-induced mouse model, established through dampness-heat exposure and HCoV-229E infection. XFBD was administered orally, followed by assessments including lung index measurement, micro-CT imaging, viral load quantification, cytokine analysis, and histological evaluation via hematoxylin-eosin staining. Proteomics and single-cell transcriptomic analyses were conducted to explore the potential mechanisms underlying XFBD’s pharmacological effects. A cellular model of HCoV-229E infection was developed to investigate changes in the cAMP/PKA signaling pathway. Molecular docking and surface plasmon resonance (SPR) experiments confirmed the strong binding affinity between key XFBD components and PKA. Finally, PKA activators and inhibitors were applied in vitro to validate these mechanistic findings. Results: In vivo studies demonstrated that XFBD significantly reduced the lung index, improved the structural integrity of lung and tongue tissues, and decreased levels of proinflammatory mediators, including IL-6, IL-8, and TNF-α. Proteomic and single-cell transcriptomic analyses showed that the differentially expressed proteins after XFBD treatment were primarily associated with inflammatory responses and immune regulation. The cAMP/PKA signaling pathway was identified as a key mechanism underlying these therapeutic effects. Notably, Western blot, ELISA, molecular docking, and SPR analyses confirmed that XFBD elevated cAMP levels and p-PKA expression, thereby activating the cAMP/PKA signaling pathway in vitro. Conclusion: This study demonstrated that XFBD significantly alleviates symptoms in mice with dampness-heat toxin pneumonia. Its therapeutic effects are mediated, at least in part, through activation of the cAMP/PKA signaling pathway. These findings provide compelling evidence that XFBD is an effective herbal remedy against HCoV-229E infection.

Objective To study the effects of macrophage migration inhibitory factor (MIF) on spinal cord injury. Methods C57BL/6 mice with injury at T9 ~T10 were taken as spinal cord injury ( SCI) model, and they were divided into the operated group and the sham oper-ated group. Immunohistochemistry was used to detect expression changes of MIF during 72 hours after operation. Reverse transcriptase-poly-merase chain reaction ( RT-PCR) was used to test changes of mRNA level. And double staining immunofluorescence techniques was used to show expressions of MIF and RhoA. Results Expression of MIF at acute stage (72 hours after injury) increased significantly. Results of RT-PCR showed that mRNA levels of MIF and RhoA both increased. There were statistical differences between the two groups (P<0. 05). Con-clusion In acute stage after SCI, MIF increased in the activated microglia. MIF accumulated in oligodendrocyte-like and astrocyte-like cells in injured spinal cord, which might contribute to inhibitory environment for regeneration. Moreover, mRNA level of MIF raised with the in-crease of RhoA mRNA level, which indicated the potential inhibition of MIF to axonal regeneration in CNS.

Objective To observe the effects of different membrane proteins and dimethylsulfoxide on neurite outgrowth of cerebellum granule cells(CGC).Methods Membrane proteins were extracted from the liver,sciatic nerve and brain white matter of adult rats and coated on the cover slips.CGC were dissociated from newborn rats and inoculated on the coated cover slips,while dimethylsulfoxide(DMSO) was added into the CGC suspension.Results The neurite outgrowth was inhibited by membrane protein of brain white mater and the effect was concentration-dependent.Low concentration(