• Journal of Food Hygiene and Safety
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• v.37 no.3
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• pp.189-197
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• 2022

Asthma is a chronic inflammatory disease characterized by recurring symptoms, airflow obstruction, and bronchial hyper-responsiveness. The onset of asthma for most patients begins early in life, and current asthma treatment with anti-inflammatory agents can have adverse effects, eventually leading to impaired quality of life. In the pathogenesis of asthma, macrophages and basophils play a vital role during progression. Macrophages not only induce inflammation by secreting inflammatory cytokines but also promote DNA damage and mucus production through nitric oxide (NO) production. Basophils enhance eosinophil recruitment and aggravate asthma through the FcεRIα receptor with high affinity for histamine and IgE. Therefore, in this study, we investigated whether the activation of macrophages and basophils is suppressed by the individual extracts of 28 natural products. RAW 264.7 cells (mouse macrophages) were treated with the natural products in LPS, and 4 natural product extracts resulted in decreased NO production. In β-hexosaminidase assay using RBL-2H3 cells (rat basophils), 19 natural product extracts decreased β-hexosaminidase production. In NO production and β-hexosaminidase assay using macrophages and basophils, 3 natural product extracts (Plantago asiatica, Centella asiatica, and Perilla frutescens var. japonica) significantly inhibited NO production and β-hexosaminidase release. Overall, we examined the inhibitory effects of 28 natural product extracts on macrophage and basophil activity, and the findings demonstrated the potential of natural product extracts for treating asthma and macrophage- and basophil-related diseases.

• Tuberculosis and Respiratory Diseases
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• v.49 no.1
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• pp.37-48
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• 2000

Backgrounds : The pathophysiology of chronic airflow obstruction, such as bronchial asthma, is characterized by mucus hypersecretion, goblet cell hyperplasia(GCH), smooth muscle hypertrophy, and inflammatory cells infiltration. In fatal asthma patients, one distinct findings is mucus hypersecretion due to GCH. However, the mechanisms of GCH in these hypersecretory diseases remain still unknown. In this study, a rat model was rapidly induced with GCH by instillation of $TiO_2$, intratracheally. We intend to confirm GCH and association of concomitant inflammatory cells infiltration and to observe the effect of potent antiinflammatory agent, that is dexamethasone, on GCH with inflammatory cells. Methods : Twenty-one 8-weeks-old male Sprague-Dawley rats were divided into three groups. Endotoxinfree water was instilled intratracheally in group 1(control) ; $TiO_2$, was instilled in the group 2 ; and dexamethasone was injected intraperitoneally to group 3 before $TiO_2$ instillation. After 120 hours, all rats were sacrificed, and trachea, bronchi, and lungs were resected respectively. These tissues were made as paraffin blocks and stained as PAS for goblet cells and Luna stain for eosinophils. We calculated the ratio of goblet cell to respiratory epithelium and number of infiltrated eosinophils from each tissue. Results : (1) Fraction of goblet cells was significantly increased in group 2 than in group 1 in the trachea and in the main bronchus. (10.19$\pm$11.33% vs 4.09$\pm$8.28%, p<0.01 and 34.09$\pm$23.91% vs 3.61$\pm$4.84%, p<0.01, respectively). (2) Eosinophils were significantly increased in the airway of group 2 than that of group 1. (5.43$\pm$3.84% vs 0.17$\pm$0.47 in trachea and 47.71$\pm$16.91 vs 2.71$\pm$1.96 in main bronchi). (3) There was a positive correlation between goblet cells and eosinophils(r=0.719, p=0.001). (4) There was significant difference in the decrease of goblet cells after dexamethasone injection between group 2 and group 3 (p<0.01). Also, infiltration of eosinophils was suppressed by dexamethasone. Conclusion : We made an animal model of $TiO_2$-induced goblet cell hyperplasia. GCH was observed mainly in the main bronchi with concomitant eosinophilic infiltration. Both goblet cell hyperplasia and eosinophilic infiltration were suppressed by dexamethasone. This animal model may serve as a useful tool in understanding of the mechanism of GCH in chronic airway diseases.