Abstract
Endothelial cells of cerebral capillaries forming the blood-brain barrier play an important role in the pathogenesis and therapy of Alzheimer’s disease. Amyloid-β peptides are key pathological elements in the development of this disease. Apigenin (4’,5,7-tetrahydroxyflavone) is a plant flavonoid and pharmacologically active agent that can be isolated from several plant species. In the present study, effects of apigenin obtained from the medicinal plant Elsholtzia rugulosa (Labiatae) on primary cultured rat cerebral microvascular endothelial cells (CMECs) mediated by amyloid-β peptide 25–35 (Aβ25–35) were examined. Aβ25–35 showed toxic effects on CMECs, involving reduction of cell viability, release of lactate dehydrogenase (LDH), increase of nuclear condensation, over-production of intracellular reactive oxygen species (ROS), decrease of superoxide dismutase (SOD) activity, and breakage of the barrier integrity and function. Based on this model, we demonstrated that apigenin from the medicinal plant Elsholtzia rugulosa protected cultured rat CMECs by increasing cell viability, reducing LDH release, relieving nuclear condensation, alleviating intracellular ROS generation, increasing SOD activity, and strengthening the barrier integrity through the preservation of transendothelial electrical resistance, permeability property and characteristic enzymatic activity after being exposed to Aβ25–35. In conclusion, apigenin isolated from Elsholtzia rugulosa has the ability to protect rat CMECs against Aβ25–35-induced toxicity.
Highlights
Cerebral microvascular endothelial cells (CMECs), contributing to form blood-brain barrier (BBB), are critical for creating and maintaining brain homeostasis, and are the primary targets in cerebral ischemic injury and neurodegenerative conditions [1,2]
Our findings indicate that apigenin isolated from Elsholtzia rugulosa had the ability to protect rat CMECs against amyloid-β peptide 25–35 (Aβ25–35)-induced toxicity
In good agreement with this notion, we observed the Aβ25–35-induced toxicity on cultured rat CMECs, involving the reduction of cell viability, the release of lactate dehydrogenase (LDH), the nuclear morphology, the overproduction of intracellular reactive oxygen species (ROS), the decrease of superoxide dismutase (SOD) activity, and the breakage of the barrier integrity and function
Summary
Cerebral microvascular endothelial cells (CMECs), contributing to form blood-brain barrier (BBB), are critical for creating and maintaining brain homeostasis, and are the primary targets in cerebral ischemic injury and neurodegenerative conditions [1,2]. Maltol glycosides and cyanogenic glycosides have been isolated from Elsholtzia rugulosa Flavonoids such as apigenin (Figure 1) are ubiquitous plant secondary metabolites and have a variety of biological effects, including anticarcinogenic, anti-inflammatory, and free radical-scavenging activities in a variety of in vitro systems, or when administered in vivo by injection [18,19,20,21,22,23]. Even though some evidence suggests that apigenin has potential effects on endothelial cells, no preexisting study has been reported the protective activity of apigenin isolated from the plant Elsholtzia rugulosa on cerebral microvascular endothelial cells mediated by amyloid-β peptide. The effects of apigenin isolated from Elsholtzia rugulosa were evaluated on Aβ-induced toxicity in the rat primary cultured cerebral microvascular endothelial cells
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