Objective:

2

To investigate the attenuating effect of Hydroxysafflor yellow A (HSYA) on inflammatory injury in chronic obstructive pulmonary disease (COPD).

Methods:

2

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:

2

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:

2

HSYA could alleviate inflammatory cell infiltration and other pathological changes in the lungs of COPD rats. HSYA could inhibit 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.