Min Xiao1, Tao Zhu, Tao Wang, Fuqiang Wen. 1. Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China/Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu 610041, China. E-mail: xiaomin_wcms@163.com.
Abstract
OBJECTIVE: To investigate the therapeutic value and possible mechanism of diammonium glycyrrhizinate (DG) in treatment of airway remodeling in a murine model of chronic asthma. METHODS: Thirty male BALB/C mice were randomly divided into control group, OVA+DG group and OVA group (n=10). HE staining was used to observe the pathological changes, and Masson's staining was used to detect and measure collagen deposition. Alpha-SMA and PPARγ mRNA expressions were analyzed by RT-PCR, and the protein expressions of α-SMA and PPARγ were measured by Western blotting. RESULTS: After 75 days of OVA sensitization and challenge, obvious pathological changes occurred in the lung tissues, which was more severe in OVA group than in OVA+DG group. Collagen deposition was significantly increased after OVA stimulation, but was obviously milder in OVA+DG group than in OVA group. OVA-induced up-regulation of α-SMA was notably attenuated by DG injection. The expression of PPARγ was markedly down-regulated after OVA stimulation but was substantially enhanced after DG intervention. CONCLUSION: DG can inhibit airway smooth muscle proliferation possibly through up-regulation of PPARγ in a murine model of chronic asthma.
OBJECTIVE: To investigate the therapeutic value and possible mechanism of diammonium glycyrrhizinate (DG) in treatment of airway remodeling in a murine model of chronic asthma. METHODS: Thirty male BALB/C mice were randomly divided into control group, OVA+DG group and OVA group (n=10). HE staining was used to observe the pathological changes, and Masson's staining was used to detect and measure collagen deposition. Alpha-SMA and PPARγ mRNA expressions were analyzed by RT-PCR, and the protein expressions of α-SMA and PPARγ were measured by Western blotting. RESULTS: After 75 days of OVA sensitization and challenge, obvious pathological changes occurred in the lung tissues, which was more severe in OVA group than in OVA+DG group. Collagen deposition was significantly increased after OVA stimulation, but was obviously milder in OVA+DG group than in OVA group. OVA-induced up-regulation of α-SMA was notably attenuated by DG injection. The expression of PPARγ was markedly down-regulated after OVA stimulation but was substantially enhanced after DG intervention. CONCLUSION: DG can inhibit airway smooth muscle proliferation possibly through up-regulation of PPARγ in a murine model of chronic asthma.