Suppression of P2X7/NF-κB pathways by Schisandrin B contributes to attenuation of lipopolysaccharide-induced inflammatory responses in acute lung injury

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• 作者：Zhiyong Cai ; Jindi Liu ; Hongliang Bian ; Jinlan Cai…
• 关键词：Schisandrin B ; Acute lung injury ; Lipopolysaccharide ; P2X7/NF ; κB
• 刊名：Archives of Pharmacal Research
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：39
• 期：4
• 页码：499-507
• 全文大小：5,284 KB
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• 作者单位：Zhiyong Cai (1)
  Jindi Liu (2)
  Hongliang Bian (1)
  Jinlan Cai (1)
  Gendi Zhu (1)
  
  1. Newborn Department, Yancheng Maternity and Child Health Care Hospital, Yancheng, 224000, Jiangsu Province, China
  2. Nursing Department, Yancheng Maternity and Child Health Care Hospital, Yancheng, 224000, Jiangsu Province, China
  
• 刊物主题：Pharmacy; Pharmacology/Toxicology;
• 出版者：Springer Netherlands
• ISSN：1976-3786

文摘

The aim of the present study was to assess the effects and mechanisms of Schisandrin B (SchB) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS (1 mg/kg), and SchB (25, 50, and 75 mg/kg) was injected 1 h before LPS challenge by gavage. After 12 h, bronchoalveolar lavage fluid (BALF) samples and lung tissues were collected. Histological studies demonstrated that SchB attenuated LPS-induced interstitial edema, hemorrhage, and infiltration of neutrophils in the lung tissue. SchB pretreatment at doses of 25, 50, and 75 mg/kg was shown to reduce LPS-induced lung wet-to-dry weight ratio and lung myeloperoxidase activity. In addition, pretreatment with SchB lowered the number of inflammatory cells and pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in BALF. The mRNA and protein expression levels of nuclear factor kappa B (NF-κB) signaling-related molecules activated by P2X7 were investigated to determine the molecular mechanism of SchB. The findings presented here suggest that the protective mechanism of SchB may be attributed partly to the decreased production of pro-inflammatory cytokines through the inhibition of P2X7/NF-κB activation.