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Matrine attenuates bleomycin-induced pulmonary injury partially via modulating mononuclear phagocyte phenotype switching in mice / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 322-328, 2017.
Article in Chinese | WPRIM | ID: wpr-506340
ABSTRACT

AIM:

To investigate the influence of matrine (MA) on the phenotype switching of mouse mono-cytes and alveolar macrophages induced by bleomycin ( BLM) .

METHODS:

All mice were randomly divided into normal saline (NS) group, BLM group, BLM+NS group and BLM +MA group.The mice were administered with BLM at 2.5 mg/kg via oropharyngeal instillation .The mice in BLM+MA group were treated with MA (15 mg· kg-1 · d-1 ) by oral gavage following BLM administration .The mice were sacrificed on days 3, 7, 14, and 21.The lungs were removed for pathological analysis .The circulating monocyte subsets and polarization state of bronchoalveolar lavage fluid ( BALF)-de-rived alveolar macrophages were analyzed by flow cytometry .

RESULTS:

The results of HE and Masson trichrome staining in BLM and BLM+NS groups exhibited classical pathological stages of lung fibrosis , including acute inflammation phase and later fibrosis phase .Compared with BLM +NS group, MA treatment alleviated the inflammatory response and the de-gree of fibrosis induced by BLM (P<0.05).There was a rapid change of circulating Ly6Chi monocytes and its magnitude was positively associated with the pulmonary inflammatory response .An expansion of M2-like alveolar macrophages was positively correlated with the magnitude of lung fibrosis .Moreover , MA treatment partially normalized the phenotype switc-hing of monocytes and alveolar macrophages .

CONCLUSION:

Matrine treatment attenuates BLM-induced pulmonary injury partially via modulating the phenotype switching of monocytes and alveolar mocrophages .

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Type: Article