Amurensin H, a Derivative From Resveratrol, Ameliorates Lipopolysaccharide/Cigarette Smoke-Induced Airway Inflammation by Blocking the Syk/NF-κB Pathway

• Main Authors: Yannan Fan (Author), Ziqian Zhang (Author), Chunsuo Yao (Author), Jinye Bai (Author), Hui Yang (Author), Pei Ma (Author), Yiyao Fan (Author), Shuyi Li (Author), Jiqiao Yuan (Author), Mingbao Lin (Author), Qi Hou (Author)
• Format: Book
• Published: Frontiers Media S.A., 2019-10-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 1663-9812; 10.3389/fphar.2019.01157
• Keywords: amurensin H; chronic obstructive pulmonary disease; airway inflammation; spleen tyrosine kinase; nuclear factor κB; Therapeutics. Pharmacology; RM1-950
• Source: Frontiers in Pharmacology, Vol 10 (2019)

Amurensin H, a resveratrol dimer derived from Vitis amurensis Rupr, has several biological effects, including anti-inflammatory and antioxidant activities. Studies have found that amurensin H attenuated asthma-like allergic airway inflammation. However, its protective activity on chronic obstructive pulmonary disease (COPD) airway inflammation is not fully explored. The present study used a lipopolysaccharide (LPS)/cigarette smoke-induced mice model and an LPS-stimulated THP-1-derived macrophages model to measure the lung tissue's morphology changes. The results showed that amurensin H ameliorated the histological inflammatory alterations in the lung tissues, leading to a decrease in the expression of interleukin 6 (IL-6), IL-17A, tumor necrosis factor α (TNF-α), and interferon γ in bronchoalveolar lavage fluid. Amurensin H also significantly inhibited the release of IL-1β, IL-6, IL-8, and TNF-α in LPS-stimulated THP-1-derived macrophages. Furthermore, amurensin H markedly inhibited the expressions of p-Syk, nuclear factor κB (NF-κB), and p-NF-κB both in vivo and in vitro. Results from cotreatment with Syk inhibitor BAY61-3606 and NF-κB inhibitor BAY11-7082 in vitro revealed that amurensin H's protective effect against airway inflammation could be due partly to the inhibition of the Syk/NF-κB pathway. These findings suggest that amurensin H shows therapeutic effects on COPD airway inflammation, and inhibiting the Syk/NF-κB pathway might be part of its underlying mechanisms.