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만성폐쇄성폐질환 동물모델에서 SGX01의 폐손상 억제 효과

Inhibitory Effects of SGX01 on Lung Injury of COPD Mice Model

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초록

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 μg/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-α, and IL-6 on L929 cells challenged with LPS. In the COPD model, SGX01 significantly inhibited the increase of neutrophils, TNF-α, IL-17A, CXCL-1, MIP2, CD8+ cells in BALF, and TNF-α, IL-1β 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.

Abstract

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 μg/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-α, and IL-6 on L929 cells challenged with LPS. In the COPD model, SGX01 significantly inhibited the increase of neutrophils, TNF-α, IL-17A, CXCL-1, MIP2, CD8+ cells in BALF, and TNF-α, IL-1β 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.

참고문헌 (36)

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