Apigenin Isolated from the Medicinal Plant Elsholtzia rugulosa Prevents β-Amyloid 25–35-Induces Toxicity in Rat Cerebral Microvascular Endothelial Cells

摘要

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.