Asperuloside and Asperulosidic Acid Exert an Anti-Inflammatory Effect via Suppression of the NF-κB and MAPK Signaling Pathways in LPS-Induced RAW 264.7 Macrophages.
Asperuloside and Asperulosidic Acid Exert an Anti-Inflammatory Effect via Suppression of the NF-κB and MAPK Signaling Pathways in LPS-Induced RAW 264.7 Macrophages.
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Asperuloside 和 Asperulosidic Acid 通过抑制 LPS 诱导的 RAW 264.7 巨噬细胞中的 NF-κB 和 MAPK 信号通路发挥抗炎作用
DOI：
10.3390/ijms19072027
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发表时间：
2018-07-12
影响因子：
5.6
通讯作者：
Liu M
中科院分区：
文献类型：
--
作者：
He J;Lu X;Wei T;Dong Y;Cai Z;Tang L;Liu M
白花蛇舌草是一种民间草药，在亚洲用于治疗炎症相关疾病。先前的研究发现，白花蛇舌草中的环烯醚萜类化合物在其抗炎活性中发挥着重要作用。本研究旨在探讨使用脂多糖 (LPS) 诱导的 RAW 264.7 细胞在白花蛇舌草中呈现的五种环烯醚萜类化合物（阿哌啶苷 (ASP)、阿哌啶酸 (ASPA)、去乙酰阿哌啶酸 (DAA)、香豆苷甲酯 (SME) 和 E-6-O-p-香豆酰香豆苷甲酯 (CSME)）的抗炎作用和潜在机制。在LPS诱导的RAW 264.7细胞中，ASP和ASPA显着降低一氧化氮（NO）、前列腺素E2（PGE2）、肿瘤坏死因子-α（TNF-α）和白介素-6（IL-6）的产生，同时抑制诱导型一氧化氮合酶（iNOS）、环氧合酶-2（COX-2）、TNF-α和IL-6 mRNA表达。 ASP 处理抑制核因子 kappaB α (IκB-α)、p38、细胞外信号调节激酶 (ERK) 和 c-Jun N 末端激酶 (JNK) 抑制剂的磷酸化。除了p38磷酸化之外，ASPA的抑制作用与ASP相似。综上所述，ASP和ASPA的抗炎作用与通过抑制NF-κB和丝裂原激活蛋白激酶（MAPK）信号通路抑制炎症细胞因子和介质有关，这为白花蛇舌草的潜在应用提供了科学证据。
Hedyotis diffusa is a folk herb that is used for treating inflammation-related diseases in Asia. Previous studies have found that iridoids in H. diffusa play an important role in its anti-inflammatory activity. This study aimed to investigate the anti-inflammatory effect and potential mechanism of five iridoids (asperuloside (ASP), asperulosidic acid (ASPA), desacetyl asperulosidic acid (DAA), scandoside methyl ester (SME), and E-6-O-p-coumaroyl scandoside methyl ester (CSME)) that are presented in H. diffusa using lipopolysaccharide (LPS)—induced RAW 264.7 cells. ASP and ASPA significantly decreased the production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in parallel with the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-6 mRNA expression in LPS-induced RAW 264.7 cells. ASP treatment suppressed the phosphorylation of the inhibitors of nuclear factor-kappaB alpha (IκB-α), p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). The inhibitory effect of ASPA was similar to that of ASP, except for p38 phosphorylation. In summary, the anti-inflammatory effects of ASP and ASPA are related to the inhibition of inflammatory cytokines and mediators via suppression of the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways, which provides scientific evidence for the potential application of H. diffusa.
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影响因子：
7.4
作者：
Reuter, Simone;Gupta, Subash C.;Chaturvedi, Madan M.;Aggarwal, Bharat B.
通讯作者：
Aggarwal, Bharat B.
影响因子：
56.9
作者：
Johnson, GL;Lapadat, R
通讯作者：
Lapadat, R
影响因子：
10.5
作者：
Mancino A;Termanini A;Barozzi I;Ghisletti S;Ostuni R;Prosperini E;Ozato K;Natoli G
通讯作者：
Natoli G
影响因子：
7.9
作者：
Li, Ao;Zhang, Xiaoxun;Wang, Yitao
通讯作者：
Wang, Yitao
影响因子：
5.1
作者：
Lin, Che-Wei;Hwang, Tsong-Long;Wu, Tian-Shung
通讯作者：
Wu, Tian-Shung