Extracts of Chrysanthemum zawadskii attenuate oxidative damage to vascular endothelial cells caused by a highly reducing sugar.

Abstract

Endothelial cells are considered candidates for involvement in the pathogenesis of diabetic vascular complications, and prevention of endothelial cell damage may be important in pharmacological attempts to prevent such complications. In the present study, I explored whether extracts of Chrysanthemum zawadskii (CZE) could prevent oxidative damage and dysfunction of a vascular endothelial cell line caused by the highly reducing sugar, 2-deoxy-D-ribose (dRib), and dysfunction of a vascular endothelial cell line. Vascular endothelial cells were treated with dRib in the presence or absence of CZE. Cell viability was monitored using a cell counting kit, and the induction of apoptosis was evaluated with a cell death kit. Prostaglandin E2 and cyclooxygenase-2 levels were measured using enzyme-linked immunosorbent assay kits. Mitochondrial membrane potential [ΔΨ(m)] was determined using a JC-1 kit. Intracellular oxidative stress was measured by fluorometric analysis of dichlorofluorescin oxidation using 2',7'-dichlorofluorescin diacetate as the probe. The expression levels of genes encoding antioxidant enzymes were analyzed by real-time polymerase chain reaction. dRib reduced cell survival and the ΔΨ(m) and markedly increased intracellular levels of reactive oxygen species and apoptosis. However, pretreatment of cells with CZE attenuated all these dRib-induced effects. The anti-oxidant N-acetyl-L-cysteine (NAC) also prevented dRib-induced oxidative cell damage. CZE attenuated the dRib-induced production of the inflammatory mediators cyclooxygenase-2 and Prostaglandin E2. NAC also exhibited anti-inflammatory effects and treatment with CZE caused transcriptional elevation of genes encoding antioxidant enzymes. Taken together, the results suggest that CZE may exert an antioxidant action that reduces dRib-induced cell damage to vascular endothelial cells and may thus aid in preventing diabetes-associated microvascular complications.