Sinomenine protects against lipopolysaccharide-induced acute lung injury in mice via adenosine A(2A) receptor signaling.
Sinomenine protects against lipopolysaccharide-induced acute lung injury in mice via adenosine A(2A) receptor signaling.
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青藤碱通过腺苷 A(2A) 受体信号传导防止脂多糖诱导的小鼠急性肺损伤。
DOI：
10.1371/journal.pone.0059257
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Dai SS
中科院分区：
文献类型：
--
作者：
Li J;Zhao L;He X;Zeng YJ;Dai SS
青藤碱（Sinomenine，SIN）是从中药青风藤（Sinomenium acutum）中提取的一种生物活性生物碱，广泛用于类风湿关节炎（RA）的临床治疗。然而，其在急性肺损伤（ALI）中的作用尚不清楚。本研究探讨SIN在脂多糖（LPS）诱导的小鼠ALI中的作用。SIN预处理组小鼠ALI后肺组织含水量和肺组织损伤程度减轻，PaO 2/FIO 2（P/F）比值显著升高。此外，SIN还能显著抑制小鼠肺组织中炎性细胞因子TNF-α和IL-1β的表达以及中性粒细胞的浸润。基因芯片分析和实时荧光定量PCR显示SIN处理上调腺苷A2 A受体（A2 AR）表达，SIN的保护作用在A2 AR基因敲除小鼠中被取消。进一步的研究证实SIN能上调A2 AR的表达，并提示A2 AR-cAMP-PKA信号通路参与SIN的抗炎作用。综上所述，这些发现证明了A2 AR相关的抗炎作用和SIN在ALI中的保护作用，这表明了治疗ALI的潜在新方法。
Sinomenine (SIN) is a bioactive alkaloid extracted from the Chinese medicinal plant Sinomenium acutum, which is widely used in the clinical treatment of rheumatoid arthritis (RA). However, its role in acute lung injury (ALI) is unclear. In this study, we investigate the role of SIN in lipopolysaccharide (LPS)-induced ALI in mice. After ALI, lung water content and histological signs of pulmonary injury were attenuated, whereas the PaO2/FIO2 (P/F) ratios were elevated significantly in the mice pretreated with SIN. Additionally, SIN markedly inhibited inflammatory cytokine TNF-α and IL-1β expression levels as well as neutrophil infiltration in the lung tissues of the mice. Microarray analysis and real-time PCR showed that SIN treatment upregulated adenosine A2A receptor (A2AR) expression, and the protective effect of SIN was abolished in A2AR knockout mice. Further investigation in isolated mouse neutrophils confirmed the upregulation of A2AR by SIN and showed that A2AR-cAMP-PKA signaling was involved in the anti-inflammatory effect of SIN. Taken together, these findings demonstrate an A2AR-associated anti-inflammatory effect and the protective role of SIN in ALI, which suggests a potential novel approach to treat ALI.
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DOI：
10.1016/j.jtcvs.2007.08.041
发表时间：
2008-01-01
影响因子：
6
作者：
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通讯作者：
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影响因子：
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影响因子：
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影响因子：
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作者：
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影响因子：
20.1
作者：
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通讯作者：
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