Methylallyl sulfone attenuates inflammation, oxidative stress and lung injury induced by cigarette smoke extract in mice and RAW264.7 cells

被引:21
|
作者
Li, Ang [1 ]
Liu, Yan [1 ]
Zhu, Xiaosong [1 ]
Sun, Xiao [1 ]
Feng, Xiuli [1 ]
Li, Dawei [3 ]
Zhang, Jiangqiang [3 ]
Zhu, Meihua [3 ]
Zhao, Zhongxi [1 ,2 ,3 ]
机构
[1] Shandong Univ, Med Sch, Inst Pharmaceut, 44 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China
[2] Shandong Engn & Technol Res Ctr Jujube Food & Dru, 44 West Wenhua Rd, Jinan 250012, Shandong, Peoples R China
[3] Shandong Freda Pharmaceut Grp Co Ltd, Shandong Prov Key Lab Mucosal & Transdermal Drug, 888 Xinluo St, Jinan 250101, Shandong, Peoples R China
关键词
Cigarette smoke; Emphysema; Antioxidant activity; Anti-inflammation; COPD; FACTOR-KAPPA-B; DIALLYL DISULFIDE; SIGNALING PATHWAY; INDUCED EMPHYSEMA; IN-VIVO; ACTIVATION; APOPTOSIS; ROS; SUPPRESSES; COPD;
D O I
10.1016/j.intimp.2018.04.028
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study, we revealed that methylallyl sulfone (AMSO2), the metabolite of active organosulfur compounds, had anti-inflammatory and antioxidant effect in a cigarette smoke extract (CSE)-induced lung injury model. Firstly, histological analysis showed that the CSE group exhibited lung injury compared with the control, which was alleviated by AMSO2. Secondly, we estimated its anti-inflammatory capacity. The results indicated that pretreatment with AMSO2 significantly decreased CSE-elevated tumor necrosis factor-alpha (TNF-alpha) and inter-leukin-6 (IL-6) in serum. Thirdly, AMSO2 also showed antioxidant properties through enhancing activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as reducing the level of malondialdehyde (MDA) and myeloperoxidase (MPO). Finally, we elucidated that AMSO2 alleviated inflammation and oxidative stress probably via suppressing ERK/p38 MAPK and inhibiting NF-kappa 3 expressions. In conclusion, we proposed that AMSO2 protected against the development of CSE-induced lung injury by reducing inflammatory cytokine levels and augmenting antioxidant activity via ERK/p38 MAPK and NF-kappa 3 pathways.
引用
收藏
页码:369 / 374
页数:6
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