Anti-inflammatory and anti-proliferative effect of herbal medicines (APR) in RAW264.7 cells

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Abstract

The objective of the present study was to analyze the effect of a mixture of medicinal plants [ Angelica gigas Nakai, Panax ginseng and Rhus verniciflua Stokes (APR)] on lipopolysaccharide (LPS)-induced inflammatory responses in the murine macrophage cell line RAW264.7. Cells were treated with APR and LPS at various concentrations and indicated times. WST assay, trypan blue assay and quantification of activated cells demonstrated that APR suppressed cell proliferation in a dose-dependent manner. APR induced G1 cell cycle arrest and inhibited the LPS-induced phosphorylation of protein kinase B (AKT), extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (p38) and necrosis factor κB (NF-κB). APR also suppressed nitric oxide synthase isoform (iNOS) and prostaglandin endoperoxide synthase 2 (Cox-2) messenger ribonucleic acid (mRNA) expression induced by LPS. Furthermore, APR decreased LPS-induced intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, as well as induced PARP and caspase-3 cleavage, suggesting that APR causes apoptosis. In conclusion, the present study indicated that APR may be advantageous in treating inflammatory disease.

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Panax ginseng.

David Kiefer, Traci Pantuso (2003)

The herbal remedies referred to as "ginseng" are derived from the roots of several plants. One of the most commonly used and researched of the ginsengs is Panax ginseng, also called Asian or Korean ginseng. The main active components of Panax ginseng are ginsenosides, which have been shown to have a variety of beneficial effects, including anti-inflammatory, antioxidant, and anticancer effects. Results of clinical research studies demonstrate that Panax ginseng may improve psychologic function, immune function, and conditions associated with diabetes. Overall, Panax ginseng appears to be well tolerated, although caution is advised about concomitant use with some pharmaceuticals, such as warfarin, oral hypoglycemic agents, insulin, and phenelzine. Panax ginseng does not appear to enhance physical performance. Products with a standardized ginsenoside concentration are available.

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Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cells via inhibiting NF-κB activation.

Jun-Feng Kou, Bo Yu, Qian Liu (2010)

Oxidative stress is a major cause in neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and cerebral ischemia. Ginsenoside Rg1, a natural product extracted from Panax ginseng C.A. Meyer, has been reported to exert notable neuroprotective activities, which partly ascribed to its antioxidative activity. However, its molecular mechanism against oxidative stress induced by exogenous hydrogen peroxide (H(2)O(2)) remained unclear. In this study, we investigated its effect on H(2)O(2)-induced cell death and explored possible signaling pathway in PC12 cells. We proved that pretreatment with Rg1 at concentrations of 0.1-10 μM remarkably reduced the cytotoxicity induced by 400 μM of H(2)O(2) in PC12 cells by MTT and Hoechst and PI double staining assay. Of note, we demonstrated the activation of NF-κB signaling pathway induced by H(2)O(2) thoroughly in PC12 cells, and Rg1 suppressed phosphorylation and nuclear translocation of NF-κB/p65, phosphorylation and degradation of inhibitor protein of κB (IκB) as well as the phosphorylation of IκB-kinase complex (IKK) by western blotting or indirect immunofluorescence assay. Besides, Rg1 also inhibited the activation of Akt and the extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the protection of Rg1 on H(2)O(2)-injured PC12 cells was attenuated by pretreatment with two NF-κB pathway inhibitors (JSH-23 or BOT-64). In conclusion, our results suggest that Rg1 could rescue the cell injury by H(2)O(2) via down-regulation NF-κB signaling pathway as well as Akt and ERK1/2 activation, which put new evidence on the neuroprotective mechanism of Rg1 against the oxidative stress and the regulatory role of H(2)O(2) in NF-κB pathway in PC12 cells. Copyright © 2010 Elsevier Ltd. All rights reserved.

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Inhibitory effect of ginsenoside Rb1 and compound K on NO and prostaglandin E2 biosyntheses of RAW264.7 cells induced by lipopolysaccharide.

Dae-Hyun Kim, Joo Yong Lee, Eun-Kyung Kim … (2005)

In this study, the antiinflammatory activities of ginsenoside Rb1, which is a main constituent of the root of Panax ginseng (Araliaceae), and of its metabolite compound K, as produced by human intestinal bacteria, on lipopolysaccharide (LPS)-induced RAW264.7 cells were investigated. Compound K potently inhibited the production of NO and prostaglandin E2 in LPS-induced RAW 264.7 cells, with IC(50) values of 0.012 and 0.004 mM, respectively. Compound K also reduced the expression levels of the inducible NO synthase (iNOS) and COX-2 proteins and inhibited the activation of NF-kB, a nuclear transcription factor. Compound K inhibited the NO level produced by iNOS enzyme activity in a cell-free system, but did not inhibit COX-1 and 2 activities. When ginsenoside Rb1 was orally administered to rats, compound K, but not ginsenoside Rb1, were excreted in their urine. These findings suggest that ginsenoside Rb1 can be transformed to compound K by intestinal bacteria, and compound K may be effective against inflammation.

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Journal ID (nlm-ta): Mol Med Rep

Journal ID (iso-abbrev): Mol Med Rep

Title: Molecular Medicine Reports

Publisher: D.A. Spandidos

ISSN (Print): 1791-2997

ISSN (Electronic): 1791-3004

Publication date (Print): May 2014

Publication date (Electronic): 10 March 2014

Publication date PMC-release: 10 March 2014

Volume: 9

Issue: 5

Pages: 1569-1574

Affiliations

Laboratory of Clinical Biology and Pharmacogenomics and Center for Clinical Research and Genomics, Institute of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea

Author notes

Correspondence to: Dr Seong-Gyu Ko, Laboratory of Clinical Biology and Pharmacogenomics and Center for Clinical Research and Genomics, Institute of Oriental Medicine, Kyunghee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea, E-mail: epiko@ 123456khu.ac.kr

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Publisher ID: mmr-09-05-1569

DOI: 10.3892/mmr.2014.2033

PMC ID: 4020494

PubMed ID: 24626965

SO-VID: c5220f4c-ec0d-49f2-a5d0-740e7dbfcb71

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This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

Anti-inflammatory and anti-proliferative effect of herbal medicines (APR) in RAW264.7 cells

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Biomarkers for Inflammatory Lung Disease

Most cited references 23

Panax ginseng.

Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cells via inhibiting NF-κB activation.

Inhibitory effect of ginsenoside Rb1 and compound K on NO and prostaglandin E2 biosyntheses of RAW264.7 cells induced by lipopolysaccharide.

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