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Article Publish Status: FREE
Abstract Title:

Isoalantolactone suppresses LPS-induced inflammation by inhibiting TRAF6 ubiquitination and alleviates acute lung injury.

Abstract Source:

Acta Pharmacol Sin. 2019 Jan ;40(1):64-74. Epub 2018 Jul 16. PMID: 30013035

Abstract Author(s):

Yun-He Ding, Yun-Duan Song, Ya-Xian Wu, Hui-Qiong He, Tian-Hong Yu, Yu-Dong Hu, De-Peng Zhang, Hong-Chao Jiang, Kai-Kai Yu, Xiao-Zong Li, Lei Sun, Feng Qian

Article Affiliation:

Yun-He Ding

Abstract:

Isoalantolactone (IAL) is a sesquiterpene lactone extracted from roots of Inula helenium L and has shown anti-inflammatory effects. In this study we investigated the therapeutic effects of IAL on acute lung injury (ALI) and elucidated the mechanisms underlying its anti-inflammation potential in vitro and in vivo. Treatment with lipopolysaccharide (LPS, 100 ng/mL) drastically stimulated production of inflammatory mediators such as NO, TNF-α, IL-1β, and IL-6 in mouse bone marrow-derived macrophages (BMDMs), which was dose-dependently suppressed by pretreatment with IAL (2.5, 5, 10, 20 μM). We further revealed that IAL suppressed LPS-induced NF-κB, ERK, and Akt activation. Moreover, the downregulation of non-degradable K63-linked polyubiquitination of TRAF6, an upstream transcription factor of NF-κB, contributed to the anti-inflammatory effects of IAL. ALI was induced in mice by intratracheal injection of LPS (5 mg/kg). Administration ofIAL (20 mg/kg, i.p.) significantly suppressed pulmonary pathological changes, neutrophil infiltration, pulmonary permeability, and pro-inflammatory cytokine expression. Our results demonstrate that IAL is a potential therapeutic reagent against inflammation and ALI.

Study Type : Animal Study

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