[Study on the mechanism of electroacupuncture in improving olfactory function in rats with allergic rhinitis-induced olfactory dysfunction through inhibition of inflammatory response].

Abstract

Objectives: To observe the effects of electroacupuncture (EA) on olfactory function, olfactory epithelial cell apoptosis, olfactory marker protein (OMP), cysteinyl aspartate-specific protease-3 (Caspase-3), and the expression of inflammatory factors in rats with allergic rhinitis (AR)-induced olfactory dysfunction, so as to explore the underlying mechanism by which EA improves olfactory function in AR-induced olfactory dysfunction.

Methods: SD rats were randomly divided into control, model and EA groups, with 8 rats in each group. AR-induced olfactory dysfunction rats model was established using ovalbumin sensitization. Bilateral "Yingxiang" (LI20) acupoints were stimulated with EA (2 Hz/15 Hz, 1 mA) for 10 min, once daily for 14 days. After the intervention, AR symptom scores of each group of rats were evaluated. Olfactory function was assessed using the buried food pellet test. HE staining was performed to observe the morphological changes in olfactory mucosa tissue. ELISA was used to detect plasma IgE, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) contents in plasma and nasal lavage fluid. Immunofluorescence staining was used to detect OMP and Caspase-3 positive expressions in olfactory mucosa. TUNEL staining was performed to detect olfactory epithelial cell apoptosis condition.

Results: Compared with the control group, rats in the model group showed significantly thinner olfactory mucosal epithelium, reduced number and disorganized arrangement of olfactory receptor neurons (ORNs), increased inflammatory cell infiltration, significantly decreased olfactory function, significantly decreased OMP expression in olfactory mucosa (P<0.01), significantly increased nasal symptom scores, plasma IgE contents, IL-1β and TNF-α contents in plasma and nasal lavage fluid, significantly increased Caspase-3 expression in olfactory mucosa (P<0.01), and significantly increased occurrence of olfactory epithelial cell apoptosis (P<0.01). Compared with the model group, rats in the EA group showed significantly thicker olfactory mucosal epithelium, increased number and more orderly arrangement of ORNs, reduced inflammatory cell infiltration, significantly improved olfactory function, significantly increased OMP expression in olfactory mucosa (P<0.01, P<0.05), significantly decreased nasal symptom scores, plasma IgE contents, IL-1β and TNF-α contents in plasma and nasal lavage fluid (P<0.05, P<0.01), significantly decreased Caspase-3 expression in olfactory mucosa (P<0.01), and significantly decreased occurrences of olfactory epithelial cell apoptosis (P<0.01).

Conclusions: EA therapy can improve olfactory function of olfactory-malfunctioned AR rat. The mechanism could be inhibition of the AR-induced damage of inflammatory cytokines to olfactory epithelium and neurons.