Abstract
Objective To observe the expression of leptin in bronchial epithelium of asthmatic rats after cigarette smoke exposure. Methods The 30 experimental rats were randomly divided into five groups, namely, normal control group(intraperitoneal injection of normal saline 1 ml), cigarette smoke control group (exposure of smoking gas lasted four weeks with 10 cigarettes per day), asthmatic model group [intraperitoneal injection of ovalbumin/Al(OH)3 mixture 1 ml], cigarette smoke asthmatic group(based on asthmatic model group, exposure of smoking gas lasted four weeks with 10 cigarettes per day), examethasone intervention group (based on smoke asthmatic group, rats were treated with intraperitoneal injection of dexamethasone 2 mg·kg-1·d-1 lasting one week), six rats in each group.Bronchoalveolar lavage fluid (BALF) were collected to detect the cell counting and classification.Pathological changes of lung tissue were observed after HE staining.Expressions of leptin was detected by Western blot and immunohistochemistry respectively.We detected the level of IL-17 in lung tissue by the method of enzyme linked immunosorbent assay. Results Compared with normal control group, the number of airway inflammation cells increased in BALF, expressions of leptin increased in lung tissues of groups of cigarette smoke control group, asthmatic model group and cigarette smoke asthmatic group.Compared with cigeratte smoke asthmatic group, the number of airway inflammation cells decreased in BALF, expressions of leptin decreased in lung tissues of groups of dexamethasone intervention group.Airway inflammation attenuated and lung tissue staining intensity reduced in groups of dexamethasone intervention group. Conclusions Cigarette smoke exposure obviously aggravate airway inflammation in asthmatic rats, and dexamethasone effectively alleviate airway inflammation, the mechanism of which may be related to leptin. Key words: Asthma; Cigarette smoke; Leptin; Dexamethasone
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