Background: Rhinitis medicamentosa, also known as ‘rebound congestion,’ is inflammation
of the nasal mucosa caused by the overuse of topical nasal decongestants. Although local
decongestants resolve the initial nasal obstruction, the overuse causes rebound obstruction. However,
how the overuse of the decongestant causes rhinitis medicamentosa is not known.
Objectives: Here, we show the intracellular effects of oxymetazoline, commonly used a local decongestant,
on the cell death pathways. We also investigated the antioxidative effects of erdosteine
suspension (175 mg/5mL), an antioxidative agent.
Methods: Thirty Wistar-albino rats were used to form the rhinitis medicamentosa model. After
rhinitis medicamentosa was clinically detected, we removed the whole lungs of animals to perform
the molecular analyses of cell death pathways.
Results: We found a statistically significant decrease in the expression levels of Atg5 (p=0.021),
Atg7 (p=0.013) and Ulk1 (p=0.036) in the oxymetazoline group compared to the control group
(p<0.05); however, Caspase 3 expression level was recorded to be significantly increased in the
oxymetazoline group, and the expression level of Beclin1 recorded to be substantially increased in
the erdosteine group (p=0.001).
Conclusion: Based on these grounds, we suggest that vasoconstriction in capillary vessels caused
by oxymetazoline could lead to a decrease in the blood supply, which triggers autophagy to ensure