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The traditional herbal medicinal product Myrrhinil-Intest® is a fixed herbal combination, which is marketed in Germany since 1959 and applied in medical practice for the treatment of gastrointestinal disorders such as functional diarrhea, irritable bowel syndrome and inflammatory bowel disease. It contains myrrh, which is described as the oleo-gum resin from mainly Commiphora molmol Engler (Burseraceae), coffee charcoal, which are the milled roasted to blackening outer seed parts of green dried Coffea Arabica Linné (Rubiaceae) fruits and chamomile flowers - the flower heads of Matricaria recutita Linné (Asteraceae). The clinical effectiveness of Myrrhinil-Intest® for the treatment of various gastrointestinal disorders was demonstrated in several clinical studies and is described in various experience reports, however its pharmacological profile is not fully elucidated. Within the present study the spasmolytic and anti-inflammatory potential of the components myrrh, chamomile and coffee charcoal was investigated. Therefore pharmacological, histological and molecular biological methods were utilised. Spasmolytic activity was characterised using isometric tension measurement with rat isolated small intestinal preparations. Anti-inflammatory potential was assessed with different methods using isolated rat small intestinal preparations and immune cell lines. Inflammation was induced with TNBS and LPS respectively. Additionally, the influence of the herbal components on the gene expression profile of native human macrophages after LPS/IFNγ stimulation was determined by microarray gene expression analysis. Chamomile flower and myrrh exerted spasmolytic effects, whereby the more pronounced spasmolytic effects of myrrh were mediated via calcium channel blockade. Myrrh and chamomile flower exerted anti-inflammatory effects.

This paper has been retracted.Shibashish Giri,1 Ulf-Dietrich Braumann,2,3 Priya Giri,1,3 Ali Acikgöz,1,4 Patrick Scheibe,3,5 Karen Nieber,6 Augustinus Bader1 1Department of Cell Techniques and Applied Stem Cell Biology, Center for Biotechnology and Biomedicine (BBZ), 2Institute for Medical Informatics, Statistics, and Epidemiology (IMISE), University of Leipzig, Leipzig, Germany; 3Interdisciplinary Center for Bioinformatics (IZBI), University of Leipzig, Leipzig, Germany; 4Klinikum St Georg, Leipzig, Germany; 5Translational Center for Regenerative Medicine (TRM Leipzig), 6Department of Pharmacology for Natural Sciences, Institute of Pharmacy, University of Leipzig, Leipzig, Germany Abstract: Much effort has been directed towards the optimization of the capture of in vivo hepatocytes from their microenvironment. Some methods of capture include an ex vivo cellular model in a bioreactor based liver module, a micropatterned module, a microfluidic 3D chip, coated plates, and other innovative approaches for the functional maintenance of primary hepatocytes. However, none of the above methods meet US Food and Drug Administration (FDA) guidelines, which recommend and encourage that the duration of a toxicity assay of a drug should be a minimum of 14 days, to a maximum of 90 days for a general toxicity assay. Existing innovative reports have used undefined extracellular matrices like matrigel, rigid collagen, or serum supplementations, which are often problematic, unacceptable in preclinical and clinical applications, and can even interfere with experimental outcomes. We have overcome these challenges by using integrated nanostructured self-assembling peptides and a special combination of growth factors and cytokines to establish a proof of concept to mimic the in vivo hepatocyte microenvironment pattern in vitro for predicting the in vivo drug hepatotoxicity in a scalable bioartificial liver module. Hepatocyte functionality (albumin, urea) was measured at days 10

Der Hirninfarkt ist einer der drei häufigsten Todesursachen in Deutschland. Er wird durch eine Unterversorgung des Gewebes mit Sauerstoff und Nährstoffen, häufig infolge von Gefäßverschlüssen, ausgelöst. Die bisher einzige Therapiemöglichkeit ist die Thrombolyse. Deshalb sind neue Therapieansätze nötig. Voraussetzung dafür sind geeignete Modelle. In dieser Arbeit wurden zellbasierte Hypoxiemodelle etabliert und charakterisiert. Es wurde der Einfluss von Sauerstoff- und/oder Glucoseentzug an humanen primären Makrophagen untersucht. Für Screeninguntersuchungen wurden neuronale und periphere (Makrophagen) Zelllinien von Ratte und Mensch verwendet. Im zweiten Teil der Arbeit wurden die Modelle genutzt, um die Wirkung von Adenin, eine rezeptorvermittelte Therapieoption, und des Phytopharmakons STW5 auf mögliche protektive Wirkungen zu untersuchen. Es wurden zellbiologische (MTT-Test, LDH-Test, DAPI-Färbung), immunologische (TNF α- ELISA, immunhistochemische Färbung), elektrophysiologische (Patch Clamp-Technik) und molekularbiologische (RT-PCR, Real-Time-PCR) Methoden angewendet. Es wurde erstmals der Adeninrezeptor an den untersuchten Zelllinien nachgewiesen und der pharmakologische Hinweis für eine bisher unbekannte humane Variante des Rezeptors erbracht. An neuronalen Zellen kam es zu einer Rezeptorinteraktion zwischen Adenin- und Adenosin-A1-Rezeptor. Antagonisten am Adeninrezeptor scheinen zur Behandlung hypoxiebedingter Zellschäden geeignet zu sein. STW5 hemmte unter hypoxischen Bedingungen die TNF α-Freisetzung humaner primärer Makrophagen. Der antiinflammatorischen Wirkung liegt die Blockierung erhöhter Kaliumströme zugrunde. An den untersuchten Zelllinien wirkte STW5 der hypoxieinduzierten Zellschädigung entgegen.