Machanism of QGG from Descurainia sophia on airway inflammation and remodeling in COPD rats / 中草药

ABSTRACT

Objective: To explore the mechanism of QGG from Descurainia sophia on the airway inflammation and remodeling in COPD rats. Methods: SD Rats were randomly divided into six groups, including control, model, QGG high (QGGH, 0.20 g/kg), medium (QGGM 0.15 g/kg), low (QGGL 0.10 g/kg) groups and aminophylline group (0.09 g/kg). Rats with COPD in the stable phase we established by exposure to tobacco smoking combined with persistent bacterial infections for eight weeks. Rat in each group were ig administrated for twenty-eight days successive five weeks after smoking. Quantitative RT-PCR was applied to determine the mRNA expression of Th17 and Treg specific transcription factors RORγt and FOXP3. Ratio of Th17/Treg was tested by flow cytometry. Apoptosis cells of lung tissue were assayed by TUNEL. The expression of apoptotic related proteins cyctoC, Caspase-9, Caspase-3, bax, bcl-2, nucleus NF-κBp65, and cytoplasm NF-κBp65 in protein extracts of lung tissue were determined by Western blotting. Results: The growth rate of control group increased obviously with weeks, however, that of model group increased slowly in COPD establishment stage and the following smoking stage. The growth rate in QGGH and aminophylline groups increased quickly from the fifth week but in QGGL and QGGM groups increased slowly. The expression of RORγt and FOXP3 was increased in model group (P < 0.05). Compared with the model group, the expression of RORγt and FOXP3 was decreased in the QGGH and positive groups (P < 0.05). The expression of CD4+IL-17+/CD4+, FOXP3+CD4+/CD4 and the ratio of CD4+IL-17+/FOXP3+CD4+ in peripheral blood was significantly increased in the model group (P < 0.05). Compared with that of model, the expression of CD4+IL-17+/CD4+, FOXP3+CD4+/CD4 and the ratio of CD4+IL-17+/FOXP3+CD4+ were decreased in the QGGH group (P < 0.05). The expression of CD4+IL-17+/CD4+, FOXP3+CD4+/CD4 was decreased in the positive group, but the ratio of CD4+IL-17+/FOXP3+CD4+ was not changed. Compared with the control group, the apoptosis of lung tissues in the model group was significantly increased. Compared with the model group, apoptosis in the QGGH and positive groups was decreased (P < 0.05). The expression of bax, cytoC, Caspase-9, Caspase-3, and nucleus NF-κBp65 were significantly increased in the lung tissues of model rats, while that of bcl-2 and cytoplasm NF-κBp65 were decreased (P < 0.05). Compared with the model group, the expression of bax, cytoC, Caspase-9, Caspase-3, and nucleus NF-κBp65 in QGGH and positive groups were obviously decreased (P < 0.05), but that of bcl-2 and cytoplasm NF-κBp65 increased (P < 0.05). Conclusion: QGG can significantly improve the survival conditions, growth ratio and pulmonary functions of rats. QGG can reduce the ratio of CD4+IL-17+/FOXP3+CD4+ in peripheral blood. It can modulate Treg and Th17 specific transcriptional factors FOXP3 and RORγt, balance the ratio of Th17/Treg. QGG can reduce the apoptosis of lung tissues, repair damaged tissue, and maintain the integrity of organ.