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

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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.

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Authors and Affiliations

  1. Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, 100029, China

    Ming Jin, Chang-jiang Xue, Yu Wang, Fang Dong, Yuan-yuan Peng, Ya-dan Zhang, Bao-xia Zang & Li Tan

Authors
  1. Ming Jin
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  2. Chang-jiang Xue
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  3. Yu Wang
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  4. Fang Dong
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  5. Yuan-yuan Peng
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  6. Ya-dan Zhang
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  7. Bao-xia Zang
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  8. Li Tan
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Contributions

Jin M designed and supervised the experiments and revised the primary manuscript. Xue CJ completed the animal experimental work and wrote the paper. Wang Y, Dong F, Peng YY, and Zhang YD took part in the animal experiment. Zang BX was responsible for HPLC analysis of HSYA. Tan L applied a part of the financial support.

Corresponding author

Correspondence to Ming Jin.

Additional information

Supported by the National Natural Science Foundation of China (No. 81270103), the Natural Science Foundation of Beijing (No. 7132047), and the Project of Integrated Traditional Chinese Medicine-Western Medicine Institute of Heart Lung and Blood Vessel Diseases

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Jin, M., Xue, Cj., Wang, Y. et al. Protective Effect of Hydroxysafflor Yellow A on Inflammatory Injury in Chronic Obstructive Pulmonary Disease Rats. Chin. J. Integr. Med. 25, 750–756 (2019). https://doi.org/10.1007/s11655-018-2577-2

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  • DOI: https://doi.org/10.1007/s11655-018-2577-2

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