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干姜(Zingiber officinalis)抑制脂多糖诱导的小鼠模型中的炎症。

Dried Ginger (Zingiber officinalis) Inhibits Inflammation in a Lipopolysaccharide-Induced Mouse Model.

机构信息

Department of Prescriptionology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2013;2013:914563. doi: 10.1155/2013/914563. Epub 2013 Jun 27.

DOI:10.1155/2013/914563
PMID:23935687
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3712229/
Abstract

Objectives. Ginger rhizomes have a long history of human use, especially with regards to their anti-inflammatory properties. However, the mechanisms by which ginger acts on lipopolysaccharide-(LPS-)induced inflammation have not yet been identified. We investigated the anti-inflammatory effects of dried Zingiber officinalis (DZO) on LPS-induced hepatic injury. Methods. ICR mice were given a DZO water extract (100, 1000 mg/kg) orally for three consecutive days. On the third day, they were administered by LPS intraperitoneally. To investigate the anti-inflammatory effects of DZO, histological, cytokine expression, and protein factor analyses were performed. Results. Oral administration of DZO significantly reduced pathological changes in the liver and proinflammatory cytokines including interferon-(IFN-) γ and interleukin-(IL-)6 in the serum. In addition, DZO inhibited LPS-induced NF- κ B activation by preventing degradation of the I κ B- α , as well as the phosphorylation of ERK1/2, SAPK/JNK, and p38 MAPKs. These were associated with a decrease in the expression of inducible nitric oxide synthase (iNOS) and cyclooxyenase-2 (COX-2). Conclusions. Our data provide evidence for the hepatoprotective mechanisms of DZO as an anti-inflammatory effect. Furthermore, use of DZO to treat could provide therapeutic benefits in clinical settings.

摘要

目的

生姜根茎在人类历史上被广泛应用,特别是其抗炎特性。然而,生姜对脂多糖(LPS)诱导的炎症的作用机制尚未确定。我们研究了干姜(DZO)水提取物对 LPS 诱导的肝损伤的抗炎作用。

方法

ICR 小鼠连续 3 天口服 DZO 水提取物(100、1000mg/kg)。第 3 天,它们经腹腔内注射 LPS。为了研究 DZO 的抗炎作用,进行了组织学、细胞因子表达和蛋白质因子分析。

结果

DZO 的口服给药显著减轻了肝脏的病理变化,并降低了血清中干扰素-γ(IFN-γ)和白细胞介素-6(IL-6)等促炎细胞因子的水平。此外,DZO 通过阻止 IκB-α的降解以及 ERK1/2、SAPK/JNK 和 p38 MAPKs 的磷酸化,抑制了 LPS 诱导的 NF-κB 激活。这与诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达减少有关。

结论

我们的数据为 DZO 的抗炎作用提供了肝保护机制的证据。此外,DZO 的使用可能为临床治疗提供治疗益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/88b2f3dc173b/ECAM2013-914563.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/bf4dadd8b570/ECAM2013-914563.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/d4495158a6b6/ECAM2013-914563.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/821575061519/ECAM2013-914563.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/883e0b414da2/ECAM2013-914563.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/576daffcd0dd/ECAM2013-914563.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/88b2f3dc173b/ECAM2013-914563.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/bf4dadd8b570/ECAM2013-914563.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/d4495158a6b6/ECAM2013-914563.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/821575061519/ECAM2013-914563.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/883e0b414da2/ECAM2013-914563.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/576daffcd0dd/ECAM2013-914563.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f800/3712229/88b2f3dc173b/ECAM2013-914563.006.jpg

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