Effects of Ergosterol on COPD in Mice via JAK3/STAT3/NF-κB Pathway
| Autor: | Wang Shumin, Wang Huan, Li Yu, Zhang Tianzhu |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male STAT3 Transcription Factor medicine.medical_specialty Immunology Cigarette Smoking Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Mice Pulmonary Disease Chronic Obstructive Internal medicine Ergosterol medicine Immunology and Allergy Animals STAT3 Dexamethasone COPD Mice Inbred ICR Lung biology Chemistry Provitamins NF-kappa B Janus Kinase 3 Lung Injury medicine.disease Malondialdehyde 030104 developmental biology medicine.anatomical_structure Endocrinology Catalase biology.protein Tumor necrosis factor alpha medicine.drug Signal Transduction |
| Zdroj: | Inflammation. 40(3) |
| ISSN: | 1573-2576 |
| Popis: | The present study was to evaluate the effect of ergosterol (ER) on CS (cigarette smoke)-induced chronic obstructive pulmonary disease (COPD) in mice. Fifty male ICR mice were randomly assigned to five groups: control group, CS group, CS + dexamethasone (Dex, 2 mg/kg) group, CS + ER (ER, 25 mg/kg) group, CS + ER (ER, 50 mg/kg). H&E staining demonstrated that ER inhibited CS-induced pathological injury in lung tissue. Besides, ER could restore the activities of superoxide dismutase (SOD) in serum and in the lung, catalase (CAT) in serum and reduce the content of malondialdehyde (MDA) in serum and in the lung. ER also inhibited pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in serum and the lung. Furthermore, ER significantly inhibited the protein expression of JAK3/STAT3/NF-κB pathway in CS-induced mice. Our findings suggested that ER might effectively ameliorate the progression of COPD via JAK3/STAT3/NF-κB pathway in mice. |
| Databáze: | OpenAIRE |
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