Objective: To evaluate effects of Epimedii Folium on airway hyperresponsiveness in rat asthma. Method: Sixty SD rats were randomly divided into 6 groups

including the normal group

asthma model group

dexamethasone group

and three Epimedii Folium groups at dose of 2.5

5.0

10.0 g· kg-1 with 10 rats in each group. A rat model of asthma was developed by ovalbumin OVA sensitization with 100 mg of OVA mixed with 100 mg aluminum hydroxide on day 0

followed by exposing to aerosolized OVA for 4 weeks. Airway reactivity was measured by Buxco's modular and invasive system. Interleukin[interferon-γ(INF-γ)

interleukin(IL) -4

IL-5

IL-6

IL-13

tumor necrosis factor-α(TNF-α) and transforming growth factor-β(TGF-β1)] levels in the bronchoalveolar lavage fluid(BALF) supernatant were analyzed by enzyme-linked immunosorhent assay(ELISA). Lung tissues were examined to evaluate the severity of inflammatory cell infiltration

airway mucus expression

and collagen deposition. Result: Compared with the normal group

OVA-expose significantly increased airway resistance of rats(RL) (P<0.01)

decreased lung dynamic compliance (Cdyn) (P<0.01)

elevated levels of IL-4

IL-5

IL-13

TGF-β1 and TNF-α

but reduced INF-γ(P<0.05

P<0.01)in the BALF

and marked increase of inflammatory cells

mucus production and collagen deposition in lung tissues (P<0.01). Compared with the model group

epimedium at the dose of 2.5

5.0

10.0 g· kg-1 significantly reduced RL

improved Cdyn (P<0.05). Epimedii Folium dose-dependently inhibited the IL-4

IL-5

and IL-13 in BALF (P<0.05

P<0.01). Histological studies showed that Epimedii Folium at the dose of 5.0

10.0 g· kg-1 markedly inhibited airway inflammation

mucus production and collagen deposition in lung tissues (P<0.05

P<0.01). Conclusion: Epimedii Folium can significantly inhibit airway hyperresponsiveness

which is associated with its alleviation on airway inflammation and remodeling.