Objective: To investigate the therapeutic effect of Quercetin on the injury vocal fold of SD rats, and to study the effect of Quercetin on the fibrosis, proliferation, migration, cell cycle of human vocal cord fibroblasts induced by transforming growth factor – _1 and its regulation of the PI3K/AKT signaling pathway.

Methods: Plate cloning experiments were used to detect the cloning ability of vocal cord fibroblasts. CCK8 was used to detect the proliferation ability of vocal cord fibroblasts. Flow cytometry was used to detect the proportion of the cell cycle. Western blot was used to detect the expression levels of key molecules such as Acta2, COL1A1, FN1, PI3K, AKT, p – PI3K, and p – AKT proteins. The vocal cord mucosa of SD rats was injured under laryngoscope. After injury, the Quercetin – treated groups were given drug treatment for 7 days. 56 days later, HE, Alcian blue, and modified EVG were used to detect the arrangement and content (hyaluronic acid, collagen fibers, and elastic fibers) of the extracellular matrix in the vocal fold of SD rats.

Results: In the cell experiment, compared with the control group, the levels of key fibrosis molecules (Acta2, COL1A1, FN1) in the TGF – _1 model group were significantly increased, the PI3K/AKT signaling pathway was activated, the cell cloning formation ability was increased, the cell proliferation and migration abilities were enhanced, and the cell cycle was arrested in the G2/M phase. Compared with the TGF – _1 model group, the Quercetin – treated groups could inhibit the expression levels of key fibrosis molecules and the activation of the PI3K/AKT signaling pathway in a dose – dependent manner, the cell cloning formation ability was decreased, the cell proliferation and migration abilities were reduced, and the cell cycle arrest was alleviated. In the animal experiment, compared with the control group, the contents of hyaluronic acid and elastic fibers in the vocal fold of SD rats in the injury group were decreased, the content of collagen fibers was increased, and the extracellular matrix was disordered. Compared with the injury group, the Quercetin – treated groups could inhibit the decrease in the contents of hyaluronic acid and elastic fibers, the increase in the content of collagen fibers, and the disorder of the extracellular matrix in the vocal fold of SD rats in a dose – dependent manner.

Conclusion: Quercetin can effectively inhibit the formation of vocal cord fibrosis. The mechanism may be related to affecting the proliferation, migration, and cell cycle of vocal cord fibroblasts by inhibiting the PI3K/AKT signaling pathway, thereby regulating the secretion of the extracellular matrix.