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Updated: Jul 12, 2026
Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
Published on: September 28, 2019
Influence of Hypericum perforatum extract and its single compounds on amyloid-beta mediated toxicity in microglial
Birgit Kraus1, Horst Wolff, Jörg Heilmann
1Chair of Phytopathology, Technical University of Munich, Wissenschaftszentrum Weihenstephan, Am Hochanger 2, Freising, Germany. birgitl.kraus@chemie.uni-regensburg.de
Abstract:
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 critical for attenuating and preventing neurodegenerative diseases. In a microglial cell line pretreated with St. John's wort (Hypericum perforatum L.) extract (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 compounds in the extract 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 concentration, 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 concentrations of fibrillar amyloid-beta (1-40) was observed. Other experiments 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 especially with the complex plant extract HPE may restore or improve microglial viability and thereby attenuate amyloid-beta mediated toxicity in Alzheimer's disease.
Insights
St. John's wort extract (HPE) protects microglia, the brain's immune cells, from amyloid-beta toxicity in Alzheimer's disease. This extract may improve microglial health and reduce neurodegeneration.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Microglia are crucial for brain health, clearing damaging amyloid-beta in Alzheimer's disease.
- Microglial survival and function are vital for preventing neurodegenerative diseases.
- Amyloid-beta aggregates are a hallmark of Alzheimer's disease, leading to neuroinflammation and cell death.
Purpose of the Study:
- To investigate the neuroprotective effects of St. John's wort extract (HPE) on microglia exposed to amyloid-beta.
- To identify specific compounds within HPE responsible for observed protective effects.
- To elucidate the mechanisms underlying HPE's potential therapeutic benefits in Alzheimer's disease models.
Main Methods:
- Utilized a microglial cell line treated with amyloid-beta (25-35) and (1-40) peptides.
- Assessed cell viability and reactive oxygen species (ROS) formation following HPE and individual compound treatment.
- Evaluated microglial phagocytic capacity and changes in cellular membrane fluidity.
Main Results:
- HPE significantly attenuated amyloid-beta-induced microglial cell death in a dose-dependent manner.
- (+)-Catechin and (-)-epicatechin, but not quercetin or its glycosides, slightly increased cell viability.
- HPE and catechins reduced amyloid-induced ROS formation, but this was not correlated with improved cell viability; phagocytosis remained unaffected.
Conclusions:
- St. John's wort extract (HPE) demonstrates in vitro neuroprotective effects against amyloid-beta toxicity in microglia.
- The beneficial effects of HPE on microglial viability may be linked to alterations in cellular membrane fluidity rather than antioxidant activity.
- HPE holds potential for therapeutic strategies aimed at restoring microglial function and mitigating Alzheimer's disease progression.
