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Updated: Mar 22, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Effect of treatment with geraniol on ovalbumin-induced allergic asthma in mice
Zheng Xue1, Xin-Guang Zhang1, Jie Wu1
1Department of Paediatrics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai, China; Shanghai University of Traditional Chinese Medicine, Shanghai, China; Pediatric Institute of Shanghai Traditional Chinese Medicine Academy, Shanghai, China.
Background:
Asthma, a complex highly prevalent airway disease, is a major public health problem for which current treatment options are inadequate.
Objective:
To evaluate the antiasthma activity of geraniol and investigate its underlying molecular mechanisms.
Methods:
In a standard experimental asthma model, Balb/c mice were sensitized with ovalbumin, treated with geraniol (100 or 200 mg/kg) or a vehicle control, during ovalbumin challenge.
Results:
Treatment of ovalbumin-sensitized/challenged mice with geraniol significantly decreased airway hyperresponsiveness to inhaled methacholine. Geraniol treatment reduced eotaxin levels in bronchoalveolar lavage fluid and attenuated infiltration of eosinophils induced by ovalbumin. Geraniol treatment reduced TH2 cytokines (including interleukins 4, 5, and 13), increased TH1 cytokine interferon γ in bronchoalveolar lavage fluid, and reduced ovalbumin-specific IgE in serum. In addition, treatment of ovalbumin-sensitized/challenged mice with geraniol enhanced T-bet (TH1 response) messenger RNA expression and reduced GATA-3 (TH2 response) messenger RNA expression in lungs. Furthermore, treatment of ovalbumin -sensitized/challenged mice with geraniol further enhanced Nrf2 protein expression and activated Nrf2-directed antioxidant pathways, such as glutamate-cysteine ligase, superoxide dismutase, and glutathione S-transferase, and enhanced formation of reduced glutathione and reduced formation of malondialdehyde in lungs.
Conclusion:
Geraniol attenuated important features of allergic asthma in mice, possibly through the modulation of TH1/TH2 balance and activation the of Nrf2/antioxidant response element pathway.
