SP-8356 inhibits acute lung injury by suppressing inflammatory cytokine production and immune cell infiltration

被引:0
|
作者
Nguyen, Thai-Uy [1 ]
Hurh, Sunghoon [1 ]
In, Soyeon [1 ]
Nguyen, Lan Phuong [1 ]
Cho, Minyeong [1 ]
Mykhailova, Kateryna [4 ]
Kim, Hong-Rae [1 ]
Ham, Byung -Joo [1 ,2 ]
Choi, Yongseok [4 ]
Kim, Won-Ki [1 ,3 ]
Hwang, Jong-Ik [1 ]
机构
[1] Korea Univ, Coll Med, Dept Biomed Sci, Seoul 02841, South Korea
[2] Korea Univ, Coll Med, Dept Psychiat, Seoul 02841, South Korea
[3] Korea Univ, Inst Inflammat Control, Seoul 02841, South Korea
[4] Korea Univ, Coll Life Sci Biotechnol, Dept Biotechnol, Seoul 02841, South Korea
关键词
SP-8356; Acute lung injury; LPS; Inflammatory cytokines; NF-KB; NF-KAPPA-B; AUTOPHAGY;
D O I
10.1016/j.intimp.2024.111847
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
This study investigated the anti-inflammatory and protective properties of SP-8356, a synthetic derivative of (1S)-(-)-verbenone, in a mouse model of LPS-induced acute lung injury (ALI). By targeting intracellular signaling pathways and inflammatory responses, SP-8356 demonstrated a potent ability to attenuate deleterious effects of proinflammatory stimuli. Specifically, SP-8356 effectively inhibited the activation of crucial signaling molecules such as NF-KB and Akt, and subsequently dampened the expression of inflammatory cytokines in various lung cellular components. Intervention with SP-8356 treatment also preserved the structural integrity of the epithelial and endothelial barriers. By reducing immune cell infiltration into inflamed lung tissue, SP-8356 exerted a broad protective effect against ALI. These findings position SP-8356 as a promising therapeutic candidate for pulmonary inflammatory diseases that cause ALI.
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页数:11
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