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| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | Life sciences | ||||
| Verlag: | Elsevier | ||||
| Band: | 81 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 11 | ||||
| Seitenbereich: | S. 884-894 | ||||
| Datum: | 2007 | ||||
| Zusätzliche Informationen (Öffentlich): | CAN 148:24236 1-11 Pharmacology 7782-44-7D (Oxygen) Role: BSU (Biological study, unclassified), BIOL (Biological study) (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia); 117-39-5 (Quercetin); 153-18-4 (Rutin); 154-23-4 ((+)-Catechin); 482-36-0 (Hyperosid); 490-46-0 ((-)-Epicatechin); 522-12-3 (Quercitrin) Role: DMA (Drug mechanism of action), PAC (Pharmacological activity), THU (Therapeutic use), BIOL (Biological study), USES (Uses) (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) | ||||
| Institutionen: | Chemie und Pharmazie > Institut für Pharmazie > Lehrstuhl Pharmazeutische Biologie (Prof. Heilmann) | ||||
| Identifikationsnummer: |
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| Stichwörter / Keywords: | Alzheimer disease Anti-Alzheimer's agents Antioxidants Hypericum perforatum Phagocytosis (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) beta -Amyloid Role: ADV (Adverse effect, including toxicity), BIOL (Biological study) (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) Reactive oxygen species Role: BSU (Biological study, unclassified), BIOL (Biological study) (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) Flavanols Flavonoids Role: DMA (Drug mechanism of action), PAC (Pharmacological activity), THU (Therapeutic use), BIOL (Biological study), USES (Uses) (Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) Cell membrane (fluidity Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) Neuroglia (microglia Hypericum perforatum ext. and compds. effect on amyloid-beta -mediated toxicity in microglia) Hypericum perforatum ext compd amyloid toxicity microglia Alzheimer's | ||||
| Dewey-Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik > 570 Biowissenschaften, Biologie 500 Naturwissenschaften und Mathematik > 540 Chemie | ||||
| Status: | Veröffentlicht | ||||
| Begutachtet: | Ja, diese Version wurde begutachtet | ||||
| An der Universität Regensburg entstanden: | Ja | ||||
| Dokumenten-ID: | 17232 |
Zusammenfassung
As immunocompetent cells of the brain, microglia are able to counteract the damaging effects of amyloid-beta in Alzheimer's disease by phagocytosis-mediated clearance of protein aggregates. The survival and health of microglia are therefore crit. for attenuating and preventing neurodegenerative diseases. In a microglial cell line pretreated with St. John's wort (Hypericum perforatum L.) ext. ...
Zusammenfassung
As immunocompetent cells of the brain, microglia are able to counteract the damaging effects of amyloid-beta in Alzheimer's disease by phagocytosis-mediated clearance of protein aggregates. The survival and health of microglia are therefore crit. for attenuating and preventing neurodegenerative diseases. In a microglial cell line pretreated with St. John's wort (Hypericum perforatum L.) ext. (HPE), the cell death evoked by treatment with amyloid-beta (25-35) and (1-40) was attenuated significantly in a dose-dependent manner. Investigation of the single compds. in the ext. revealed that the flavanols (+)-catechin and (-)-epicatechin increase cell viability slightly, whereas the flavonol quercetin and its glycosides rutin, hyperosid and quercitrin showed no effect on cell viability. In contrast, at the same concn., the flavonoids reduced the formation of amyloid-induced reactive oxygen species in microglia, indicating that improvement of cell viability by the catechins is not correlated to the antioxidant activity. No influence of HPE on the capacity of microglia to phagocytose sub-toxic concns. of fibrillar amyloid-beta (1-40) was obsd. Other expts. showed that HPE, (+)-catechin and (-)-epicatechin can alter cellular membrane fluidity and thereby may have a beneficial effect on cell health. Our findings provide in vitro evidence that treatment esp. with the complex plant ext. HPE may restore or improve microglial viability and thereby attenuate amyloid-beta mediated toxicity in Alzheimer's disease.
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