Menthol citrate ester (MC) is a chemically defined menthol-derived compound, but its inhalation safety and timing-dependent effects on allergic airway inflammation remain unclear. Here, the inhalation safety and biological effects of aerosolized MC were evaluated through in vitro and in vivo approaches. Acute inhalation exposure resulted in no mortality, exposure-related clinical signs, hematological or biochemical alterations, or evident histopathological injury in mice, while MC maintained cytocompatibility in RAW264.7 cells at concentrations up to 500 μg/mL. In an ovalbumin (OVA)-induced allergic airway inflammation model, post-challenge MC treatment reduced serum total and OVA-specific immunoglobulin E (IgE), suppressed IL-13, IL-5, IL-33, TSLP, CCL11, IL-6, and IL-1β levels in bronchoalveolar lavage fluid (BALF), and decreased eosinophil and neutrophil accumulation. Histological analyses showed reduced airway inflammation, mucus hypersecretion, and collagen deposition. In contrast, pre-challenge administration failed to provide protection and further increased several inflammatory indices. Bulk RNA sequencing showed that high-dose therapeutic MC partially reversed OVA-induced transcriptional programs associated with epithelial alarmin signaling, type 2 inflammation, eosinophil recruitment, mucus production, airway remodeling, inflammatory amplification, and sensory-response regulation. Quantitative polymerase chain reaction (qPCR) confirmed downregulation of Il33, Il1rl1, Mmp9, and Htr3a, while Western blotting showed reduced IL-33, ST2/IL1RL1, MMP9, and HTR3A protein expression. These findings support the preliminary inhalation safety of MC and demonstrate a timing-dependent therapeutic effect in established allergic airway inflammation.

Bacterial cellulose-chloramphenicol (BC-Chl) composite membranes have been prepared using an impregnation-recrystallization method by loading chloramphenicol on bacterial cellulose. The morphology and structure of the composite membranes were characterized by scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FT-IR) and X-ray diffraction (XRD). The results show that the BC-Chl composite membrane maintains the porous three-dimensional network structure of bacterial cellulose. The loading of chloramphenicol did not change the crystal form of the bacterial cellulose, but the loading process did destroy the crystalline region of the cellulose to a certain extent. After swelling for 12 h, the swelling ratio of the BC-Chl composite membrane was above 400%, showing its good water retention capacity. In vitro drug release experiments showed that the drug concentration peak time of the BC-Chl composite membrane was extended to about 2 h compared with 45 min for the chloramphenicol raw material, confirming a delayed drug release effect. Inhibition zone tests showed that when the drug loading was about 200 μg/mg, the inhibition zone diameter rates of the BC-Chl composite membrane against Corynebacterium glutamicum and Escherichia coli were 5.8 and 5.1, respectively. After SH-SY5Y cells were treated with the BC-Chl composite membrane with a drug loading of about 200 μg/mg for 24 h, the cell activity remained above 75%, indicating that the BC-Chl composite membrane had low cytotoxicity and good biocompatibility.