Protective Effect of Hydroxysafflor Yellow A on Inflammatory Injury in Chronic Obstructive Pulmonary Disease Rats.
10.1007/s11655-018-2577-2
- Author:
Ming JIN
1
;
Chang-Jiang XUE
2
;
Yu WANG
2
;
Fang DONG
2
;
Yuan-Yuan PENG
2
;
Ya-Dan ZHANG
2
;
Bao-Xia ZANG
2
;
Li TAN
2
Author Information
1. Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China. jm64456308@163.com.
2. Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China.
- Publication Type:Journal Article
- Keywords:
Hydroxysafflor yellow A;
chronic obstructive pulmonary disease;
inflammation;
nuclear factor-κB;
p38 mitogen-activated protein kinase
- From:
Chinese journal of integrative medicine
2019;25(10):750-756
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the attenuating effect of Hydroxysafflor yellow A (HSYA) on inflammatory injury in chronic obstructive pulmonary disease (COPD).
METHODS:Rats were randomly assigned to 7 groups according to body weight including normal control group, HSYA blank group (76.8 mg/kg), COPD group, COPD+HSYA (30, 48, 76.8 mg/kg) groups and COPD+dexamethasone (2 mg/kg), 10 in each group. Passive cigarette smoke and intratracheal instillation of lipopolysaccharides were used to establish a COPD model in rats. Hematoxylin and eosin staining of lung tissue sections was used, real-time polymerase chain reaction (PCR) was used to assay mRNA levels of some cytokines in lung tissues, the cytokines in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA), Western blot analysis was used to determine phosphorylated p38 mitogen-activated protein kinase (MAPK) levels in lung tissues, and nuclear factor-κB (NF-κB) p65 protein levels in lung tissues were detected by immunohistochemistry.
RESULTS:Lung alveolar septa destruction, alveolus fusion, inflammatory cell infiltration, and bronchiole exudation were observed. These pathological changes were alleviated in the COPD+HSYA group. The mRNA expression of inflammatory factors were significantly increased in lung tissues from COPD rats (all P<0.01) and were inhibited by HSYA. Levels of inflammatory cytokines in BALF of COPD rats were significantly increased (all P<0.01) which were inhibited by HSYA (all P<0.01, 48, 76.8 mg/kg). The levels of p38 MAPK phosphorylation and p65 in lung tissues of COPD rats were significantly increased (all P<0.01) and were suppressed by HSYA (all P<0.01, 48, 76.8 mg/kg).
CONCLUSIONS:HSYA could alleviate inflammatory cell infiltration and other pathological changes in the lungs of COPD rats. HSYA inhibited inflammatory cytokine expression, and increase phosphorylation of p38 MAPK and NF-κB p65 in the lungs of COPD rats. The protective mechanism of HSYA to inhibit COPD inflammation might be by attenuating NF-κB and p38MAPK signal transduction.
