Abstract

The mechanism of baicalin in airway reconstruction in rats with chronic obstructive pulmonary disease was investigated. The chronic obstructive pulmonary disease models were established in rats through smoke inhalation and instilling lipopolysaccharide. The rats were then divided into the control group and the experimental group, a blank group was used as a reference point of the experiment. Rats in the experiment group received baicalin either at a high dose (80 mg/kg/d, H1) or at a low dose (25 mg/kg/d, H2) to analyze the airway reconstruction functions and antiinflammatory effects of baicalin. During the experiment, the general conditions of the rats were compared. After the experiment, lung tissues of the rats were obtained for Hematoxylin-Eosin staining, and the pathological changes were observed. In addition, the bronchial walls were measured and analyzed. Using immunohistochemical staining, the expression levels of tumor necrosis factor-α and interferon-γ in rat lung tissues were analyzed and compared. Hematoxylin-Eosin staining of lung tissues showed that the rats with chronic obstructive pulmonary disease had severe pathological damages; compared to the blank group, while in rats treated with baicalin, bronchial obstruction, alveolar structure and inflammatory infiltration were improved, and the differences were statistically significant (p<0.05). After baicalin administration, the bronchial wall thickness in chronic obstructive pulmonary disease rats was reduced, collagen deposition in the bronchial epithelium was improved, and airway smooth muscle proliferation was alleviated compared to the control group. Baicalin intervention at high dose decreased the expressions of TNF-α and IFN-γ in chronic obstructive pulmonary disease rats as well as the ratio of Th17/Treg in the lung tissues and improved the balance of the ratio of Th17/Treg. In addition, baicalin treatment reduced the positive cell count of RORγt in the lung tissues of the chronic obstructive pulmonary disease rats, and all these differences were statistically significant (p<0.05). In summary, baicalin administration inhibited airway reconstruction of the chronic obstructive pulmonary disease rats, and the mechanism of the antiinflammatory effect of baicalin appeared to be through the regulation of TNF-α and IFN-γ in lung tissues.