Anti-inflammatory action of physalin A by blocking the activation of NF-κB signaling pathway,Journal of Ethnopharmacology

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Anti-inflammatory action of physalin A by blocking the activation of NF-κB signaling pathway
Journal of Ethnopharmacology ( IF 4.8 ) Pub Date : 2020-10-19 , DOI: 10.1016/j.jep.2020.113490
Liying Wang ₁ , Jinpo Gu ₂ , Mingyue Zong ₁ , Qingran Zhang ₁ , Huixiang Li ₁ , Danna Li ₁ , Xiaofeng Mou ₁ , Pan Liu ₁ , Yanan Liu ₁ , Feng Qiu ₃ , Feng Zhao ₁

Affiliation

Ethnopharmacological relevance

Physalis Calyx seu Fructus typically used to treat inflammatory diseases such as upper respiratory tract infection and acute tonsillitis in clinical practice of China. Physalin A, a main active ingredient of this TCM, has been reported for its significant anti-tumor activity. However, most reports focused on the studies of its anti-tumor activity, the anti-inflammatory activity of physalin A and its molecular mechanism are still not elucidated clearly.

Aim of the study

The aim of the study was to investigate the anti-inflammatory activities both in vitro and in vivo and molecular mechanism of physalin A.

Materials and Methods

The potential anti-inflammatory properties of physalin A were evaluated in vitro by lipopolysaccharide (LPS)-induced RAW 264.7 macrophages cells, and in vivo via two typical acute inflammation murine models. Some important inflammation-related molecules were analyzed by enzyme-linked immuno sorbent assay (ELISA) and Western blotting.

Results

The results showed that physalin A inhibited carrageenan-induced paw edema and capillary permeability of mice induced by acetic acid in vivo. Furthermore, physalin A also significantly reduced the release of inflammatory mediators nitric oxide (NO), prostaglandin E2 (PGE₂), and tumor necrosis factor-α (TNF-α) induced by lipopolysaccharide (LPS) in RAW 264.7 in vitro. Further investigations indicated that physalin A can down-regulate the high expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Physalin A remarkably blocked the degradation of inhibitor of nuclear factor kappa B alpha (IκB-α) and the nuclear translocation of nuclear factor-κB (NF-κB) p65 induced by LPS in RAW 264.7 cells. However, physalin A did not significantly inhibit the phosphorylation of mitogenactivated protein kinases (MAPKs) family proteins c-Jun N-terminal kinases (JNK) or extracellular signal-regulated kinase (ERK) or p38.

Conclusions

All the results clearly illustrated that the anti-inflammatory action of physalin A is due to the inactivation of NF-κB signal pathway, but is irrelevant to the MAPKs pathway.

中文翻译：

physalin A 通过阻断 NF-κB 信号通路的激活发挥抗炎作用

民族药理学相关性

酸浆在我国临床上通常用于治疗上呼吸道感染、急性扁桃体炎等炎症性疾病。酸浆素 A 是该中药的主要活性成分，据报道具有显着的抗肿瘤活性。然而目前的研究大多集中于其抗肿瘤活性的研究，而酸浆素A的抗炎活性及其分子机制尚未阐明。

研究目的

本研究的目的是探讨 physalin A 的体外和体内抗炎活性及其分子机制。

材料和方法

酸浆蛋白 A 的潜在抗炎特性通过脂多糖 (LPS) 诱导的 RAW 264.7 巨噬细胞进行体外评估，并通过两种典型的急性炎症小鼠模型进行体内评估。通过酶联免疫吸附测定（ELISA）和蛋白质印迹分析一些重要的炎症相关分子。

结果

结果表明，酸浆蛋白A可抑制角叉菜胶引起的小鼠足肿胀和醋酸引起的体内毛细血管通透性。此外，在体外RAW 264.7中，酸浆素A还显着减少脂多糖（LPS）诱导的炎症介质一氧化氮（NO）、前列腺素E2（PGE ₂ ）和肿瘤坏死因子-α（TNF-α）的释放。进一步的研究表明，physalin A 可以剂量依赖的方式下调诱导型一氧化氮合酶 (iNOS) 和环氧合酶-2 (COX-2) 的高表达。 Physalin A 显着阻断 RAW 264.7 细胞中 LPS 诱导的核因子 kappa B α (IκB-α) 抑制剂的降解和核因子 -κB (NF-κB) p65 的核转位。然而，酸浆蛋白 A 不会显着抑制丝裂原激活蛋白激酶 (MAPK) 家族蛋白 c-Jun N 末端激酶 (JNK) 或细胞外信号调节激酶 (ERK) 或 p38 的磷酸化。