Hindawi Publishing Corporation Evidence-Based Complementary and Alternative Medicine Volume 2012, Article ID 983023, 10 pages doi:10.1155/2012/983023 Research Article Selected Extracts of Chinese Herbal Medicines: Their Effect on NF-κB, PPARα and PPARγ and the Respective Bioactive Compounds E. Rozema, 1 A. G. Atanasov, 1 N. Fakhrudin, 1, 2 J. Singhuber, 1 U. Namduang, 1 E. H. Heiss, 1 G. Reznicek, 1 C. W. Huck, 3 G. K. Bonn, 3 V. M. Dirsch, 1 and B. Kopp 1 1 Department of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria 2 Department of Pharmaceutical Biology, Faculty of Pharmacy, Gadjah Mada University, Sekip Utara, Yogyakarta 55281, Indonesia 3 Institute of Analytical Chemistry and Radiochemistry, University of Innsbruck, Innrain 52a, 6020 Innsbruck, Austria Correspondence should be addressed to B. Kopp, brigitte.kopp@univie.ac.at Received 21 February 2012; Accepted 13 March 2012 Academic Editor: Olumayokun A. Olajide Copyright © 2012 E. Rozema et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Chinese herbal medicinal (CHM) extracts from fourteen plants were investigated in cell-based in vitro assays for their effect on nuclear factor κB (NF-κB), a key regulator of inflammation, as well as on peroxisome proliferator-activated receptors (PPARs) being key regulators of genes involved in lipid and glucose metabolism. 43% of the investigated CHMs showed NF-κB inhibitory and 50% PPARα and PPARγ activating effects. Apolar extracts from cortex and flos of Albizia julibrissin Durazz. and processed rhizomes of Arisaema sp. and Pinellia ternata (Thunb.) Breit. that effectively inhibited TNF-α-induced NF-κB activation and dose- dependently activated PPARα and PPARγ were further investigated. Bioassay-guided fractionation and analysis by GC-MS led to the identification of fatty acids as PPAR agonists, including linoleic and palmitic acid. 1. Introduction Herbal medicines are an important part of Traditional Chinese Medicine (TCM) of which the medical use and pro- cessing methods are well documented. Traditional processing methods (pao zhi) are important to enhance the efficacy and/or to reduce the toxicity of crude herbal products [1]. Chinese herbal medicine (CHM) encompasses over 11,000 species of medicinal plants and is a valuable source [2] for the identification of biologically active natural products. Investigation of the molecular targets and mechanistic action of CHMs and their single compounds is currently a central task in TCM research [3]. Thanks to advances in molecular biology, refined bioassays are now available which enable rapid screening of natural products for bioactivity towards specific targets [4]. In this study, extracts of different polarity from CHMs of fourteen plant species were tested for a potential inhibition of TNF-α-induced NF-κB activation and an agonistic activity towards PPARα and PPARγ. The CHMs were selected in cooperation with Chinese partners [5]. This in-house collection of CHMs (Table 1) was already examined earlier based on their traditional use against insomnia and anxiety regarding a putative modulation of the GABA A receptor [6]. The listed CHMs are, however, also traditionally prescribed as single herbs as well as in formulations for clearing heat and drying dampness, among others. Therefore, to gain insight into possible multi-target effects of the individual CHMs, this study examined their influence on the nuclear factor κB (NF-κB) pathway and peroxisome proliferator-activated receptors (PPARs), which are impor- tant drug targets with regard to inflammation and metabolic dysfunction. The NF-κB signaling pathway is a key regulator of inflammation. Inflammatory stimuli such as tumor necrosis factor alpha (TNF-α), infectious agents (lipopolysaccharide (LPS)), injury, and other stressful conditions activate the NF-κB signal transduction pathway. Thereby, activation of the IKK complex leads to phosphorylation and subsequent proteasomal degradation of IκB proteins. NF-κB dimers are translocated to the nucleus and bind to κB promotor