Propofol Exerted an Anti-Asthmatic Effect by Attenuating Extracellular Matrix Deposition and Viability of Airway Smooth Muscle Cells.

INTRODUCTION

Propofol is the preferred anaesthetic for asthma patients due to its bronchodilatory effects, yet its protective mechanisms remain unclear. This study investigated its effects both in vivo and in vitro.

METHODS

An asthmatic mouse model was induced using ovalbumin (OVA). Airway responsiveness, lung histopathology, and inflammatory biomarkers (IgE, IL-4, IFN-γ) were assessed. TGF-β1-stimulated airway smooth muscle (ASM) cells were used for proliferation, migration, and apoptosis assays via MTT, Transwell, and flow cytometry. ECM production was analyzed by immunohistochemistry and immunofluorescence. The SAPK/JNK signaling pathway was evaluated by western blot.

RESULTS

Propofol dose-dependently attenuated airway hyperresponsiveness and lung histological damage in OVA-induced asthmatic mice, while reversing abnormal inflammatory biomarker expression. In vitro, propofol inhibited ASM cell proliferation and migration and promoted apoptosis. It also suppressed ECM synthesis and restored TIMP-1 expression to rebalance ECM homeostasis. Mechanistically, propofol inhibited SAPK/JNK pathway activation in both in vivo and in vitro models.

DISCUSSION: These findings clarify the molecular mechanisms underlying Propofol's protective effects, providing a foundation for its potential therapeutic use in asthma treatment.