Thymol, a naturally occurring monocyclic phenolic compound derived from Thymus vulgaris (Lamiaceae), has been reported to exhibit anti-inflammatory property in vivo and vitro. However, the mechanism of
thymol is not clear. The aim of the present study was to investigate the effects of
thymol on allergic
inflammation in OVA-induced mice
asthma and explore its mechanism. The model of mouse
asthma was established by the induction of OVA.
Thymol was orally administered at a dose of 4, 8, and 16 mg/kg
body weight 1h before OVA challenge. At 24h after the last challenge, mice were sacrificed, and the data were collected by various experimental methods. The results revealed that pretreatment with
thymol reduced the level of OVA-specific
IgE, inhibited recruitment of inflammatory cells into airway, and decreased the levels of
IL-4,
IL-5, and
IL-13 in BALF. Moreover, the pathologic changes of lung tissues were obviously ameliorated and goblet cell
hyperplasia was effectively inhibited by the pretreatment of
thymol. In addition,
thymol reduced the development of
airway hyperresponsiveness and blocked the activation of NF-κB pathway. All data suggested that
thymol ameliorated airway
inflammation in OVA-induced mouse
asthma, possibly through inhibiting NF-κB activation. These findings indicated that
thymol may be used as an alternative agent for treating allergic
asthma.