만성폐쇄성폐질환 동물모델에서 SGX01의 폐손상 억제 효과
Objective: This study aimed to evaluate the inhibitory effects of SGX01 on the lung injuries of COPD mice model. Materials and Methods: This study was carried out in two ways: in vitro and in vivo. In vitro, L929 cells were challenged with LPS, and then treated with six concentrations of SGX01 (10,...
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Published in: | 대한한방내과학회지 Vol. 40; no. 4; pp. 567 - 581 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | Korean |
Published: |
대한한방내과학회
01-09-2019
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Subjects: | |
Online Access: | Get full text |
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Summary: | Objective: This study aimed to evaluate the inhibitory effects of SGX01 on the lung injuries of COPD mice model. Materials and Methods: This study was carried out in two ways: in vitro and in vivo. In vitro, L929 cells were challenged with LPS, and then treated with six concentrations of SGX01 (10, 30, 50, 100, 300, and $500{\mu}g/ml$) and analyzed by ELISA. In vivo, C57BL/6 mice were challenged with LPS and cigarette smoking solution (CSS), and then treated with a vehicle only (control group), dexamethasone 3 mg/kg (dexa group), or a SGX01 200 mg/kg (SGX01 group). After sacrifice, the BALF or lung tissue was analyzed with Cytospin, FACS, ELISA, real-time PCR and H&E, and Masson's trichrome staining. Results: SGX01 significantly decreased NO, $TNF-{\alpha}$, and IL-6 on L929 cells challenged with LPS. In the COPD model, SGX01 significantly inhibited the increase of neutrophils, $TNF-{\alpha}$, IL-17A, CXCL-1, MIP2, CD8+ cells in BALF, and $TNF-{\alpha}$, $IL-1{\beta}$ mRNA expression in lung tissue. It also decreased the severity of the histological lung injury. Conclusion: This study suggests the usability of SGX01 for COPD patients by controlling lung tissue injury. |
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Bibliography: | KISTI1.1003/JNL.JAKO201930352304345 |
ISSN: | 1226-9174 |
DOI: | 10.22246/jikm.2019.40.4.567 |