OBJECTIVETo observe the expression of tumor necrosis factor-alpha (TNF-α) protein in the lung tissue of rats with chronic obstructive pulmonary disease (COPD), and to evaluate the intervention and mechanism of Heche Chongcao Capsule (HCC).

METHODSThe COPD rat model was prepared by exposure to cigarettes smoke plus intratracheal injecting lipopolysaccharide (LPS). Forty successfully modeled SD rats were randomly divided into the COPD model group, the control group, the low dose HCC group, the medium dose HCC group, and the high dose HCC group, 8 in each group. Meanwhile, a normal control group consisting of 6 rats was also set up. HCC at 0.25, 0.5, and 1.0 g/kg was administered to rats in the 3 dose HCC groups respectively by gastrogavage combined with Theophylline Sustained Release Tablet (TSRT). Rats in the control group were administered with TSRT by gastrogavage at 4.5 mg/kg, 1 mL/100 g each time, once daily. All medication lasted for 4 successive weeks. Equal volume of distilled water was administered by gastrogavage to rats in the COPD model group and the normal control group. Morphological changes of the lung tissue were observed under microscope. The expression of TNF-α protein in the lung tissue were also detected using Real-time PCR.

RESULTSUnder electron microscope, the cilium in the tracheal epithelium was disorderly arranged, type I and II alveolar cells were degenerated, endoplasmic reticulum and mitochondria were swollen, the lamellar body was emptied, and free fragment could be seen inside alveolar space. Compared with the model group, all lesions were somewhat ameliorated in all medicated groups, especially in the medium dose HCC group. Compared with the model group, the expression of TNF-α protein decreased in all medicated groups, especially in the medium and low dose HCC groups (P < 0.05, P < 0.01). Compared with the control group, the expression of TNF-α protein decreased in the medium and low dose HCC groups (P < 0.05).

CONCLUSIONHCC could effectively regulate the expression of TNF-α protein and inhibit airway inflammation reaction in COPD rats.