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Protective Effect of Hydroxysafflor Yellow A on Inflammatory Injury in Chronic Obstructive Pulmonary Disease Rats

  • Ming JinEmail author
  • Chang-jiang Xue
  • Yu Wang
  • Fang Dong
  • Yuan-yuan Peng
  • Ya-dan Zhang
  • Bao-xia Zang
  • Li Tan
Original Article
  • 14 Downloads

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.

Keywords

Hydroxysafflor yellow A chronic obstructive pulmonary disease inflammation p38 mitogen-activated protein kinase nuclear factor-κB 

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Copyright information

© Chinese Association of the Integration of Traditional and Western Medicine 2018

Authors and Affiliations

  • Ming Jin
    • 1
    Email author
  • Chang-jiang Xue
    • 1
  • Yu Wang
    • 1
  • Fang Dong
    • 1
  • Yuan-yuan Peng
    • 1
  • Ya-dan Zhang
    • 1
  • Bao-xia Zang
    • 1
  • Li Tan
    • 1
  1. 1.Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical UniversityBeijing Institute of Heart Lung and Blood Vessel DiseasesBeijingChina

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