the General Program of National Natural Science Foundation of China(81670018);the National Natural Science Foundation for Young Scholars of China(81600022)
Yaping WANG, Wenjing ZOU, Shuang CAI, et al. Menthol improves airway inflammation and hyperresponsiveness in asthmatic mice by reducing substance P in the lungs[J]. Journal of Third Military Medical University, 2017, 39(22): 2151-2156.
DOI:
Yaping WANG, Wenjing ZOU, Shuang CAI, et al. Menthol improves airway inflammation and hyperresponsiveness in asthmatic mice by reducing substance P in the lungs[J]. Journal of Third Military Medical University, 2017, 39(22): 2151-2156. DOI: 10.16016/j.1000-5404.201707119.
Menthol improves airway inflammation and hyperresponsiveness in asthmatic mice by reducing substance P in the lungs
To investigate the effect of aerosol inhalation of menthol on airway inflammation
airway hyperresponsiveness and substance P content in the lungs of asthmatic mice.
Methods
2
Thirty female BALB/c mice aged 6-8 weeks were randomly divided into control group
asthma group and menthol treatment group. In the latter 2 groups
the mice were challenged with chicken ovalbumin (OVA) for 10 consecutive days to induce asthma; in menthol treatment group
the mice received inhalation of 5 mL 1.6% menthol solution for 30 min before each challenge. The mice in the control group were treated with PBS only. Within 24 h following the last challenge
the airway hyperresponsiveness (AHR) of the mice was assessed
and the total cell count and eosinophil count in the bronchoalveolar lavage fluid (BALF) were determined within 48 h. HE staining was used to observe the pathological changes in the lungs
and ELISA was used to detect the levels of serum total immunoglobulin E (IgE) and substance P in the lung homogenate; the expression of substance P in the lung tissue was also detected using immunohistochemistry.
Results
2
The asthmatic mice showed a significantly higher level of AHR than the control mice (
P
<
0.05)
and menthol treatment obviously ameliorated AHR in asthmatic mice (
P
<
0.05). The total cell and eosinophil counts in the BALF in asthmatic mice were significantly increased as compared with those in the control group (
P
<
0.001)
and were obviously lowered by menthol treatment (
P
<
0.01). HE staining of the lungs of asthmatic mice revealed obvious inflammatory cell infiltration
which was significantly lessened in menthol-treated mice. Compared with the control group
the asthmatic mice showed significantly elevated serum total IgE level and substance P content in the lung homogenate (
P
<
0.01)
and these elevations were obviously reduced in menthol treatment group (
P
<
0.05). Immunohistochemistry revealed strong expressions of substance P in the airway epithelium and the perivascular tract
but the lung tissues of menthol-treated mice showed only moderate substance P expression.
Conclusion
2
Aerosol inhalation of menthol can reduce airway inflammation and airway hyperresponsiveness in asthmatic mice possibly in relation to its effect of reducing substance P content and neurogenic inflammation in the lungs.
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