Mi Kyoung Moon

Anti-Inflammatory Effect of Buddleja officinalis on Vascular Inflammation in Human Umbilical Vein Endothelial Cells

Vascular inflammation process has been suggested to be an important risk factor in the initiation and development of atherosclerosis. In this study, we investigated whether and by what mechanisms an aqueous extract of Buddleja officinalis (ABO) inhibited the expressions of cellular adhesion molecules, which are relevant to inflammation and atherosclerosis. Pretreatment of human umbilical vein endothelial cells (HUVEC) with ABO (1-10 microg/ml) for 18 hours dose-dependently inhibited TNF-alpha-induced adhesion U937 monocytic cells, as well as mRNA and protein expressions of vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1). Pretreatment with ABO also blocked TNF-alpha-induced ROS formation. Nuclear factor-kappa B (NF-kappaB) is required in the transcription of these adhesion molecule genes. Western blot analysis revealed that ABO inhibits the translocation of the p65 subunit of NF-kappaB to the nucleus. ABO inhibited the TNF-alpha-induced degradation of IkappaB-alpha, an inhibitor of NF-kappaB, by inhibiting the phosphorylation of IkappaB-alpha in HUVEC. Taken together, ABO could reduce cytokine-induced endothelial adhesiveness throughout down-regulating intracellular ROS production, NF-kappaB, and adhesion molecule expression in HUVEC, suggesting that the natural herb Buddleja officinalis may have potential implications in atherosclerosis.

Effect of Benincasa hispida Cogniaux on high glucose-induced vascular inflammation of human umbilical vein endothelial cells

Vascular inflammation is an important factor which can promote diabetic complications. Preliminary investigations of several crude plant extracts including aqueous extract of Benincasa hispida Cogniaux exhibit anti-inflammatory properties. This study investigates the mechanism of anti-vascular inflammatory activity of an aqueous extract of B. hispida Cogniaux (ABH) in human umbilical vein endothelial cells (HUVECs). The study was performed on HUVECs that were pretreated with various concentrations (1-20 microg/ml) of ABH before exposure with high glucose (25 mM) for 48 h. Cell ELISA and Western blot analysis showed that ABH inhibited high glucose-induced cell adhesion molecules (CAMs) surface and protein expression, resulting in reduced adhesion of U937 monocytes. ABH also inhibited the mRNA expression level of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). High glucose-induced ROS production was inhibited by treatment of ABH. We observed that pretreatment with HUVECs with ABH blocks NF-kappaB activation via blocking phosphorylation and degradation of its inhibitory protein, IkappaB-alpha. ABH also reduced NF-kB promoter activity. These results suggest that ABH reduces high glucose-induced CAMs activation by inhibiting monocyte adhesion, ROS, and NF-kappaB in HUVECs.

Anti-Atherogenic Effects of the Aqueous Extract of Rhubarb in Rats Fed an Atherogenic Diet

The present study was designed to investigate whether the aqueous extract of rhubarb (AR) could prevent the development of atherosclerosis through regulating vascular inflammatory processes in rats fed with an atherogenic diet. AR significantly reduced plasma low-density lipoprotein-cholesterol, and increased plasma high-density lipoprotein-cholesterol in rats fed with an atherogenic diet. AR inhibited vascular expressions of endothelin-1 (ET-1) and endothelin-converting enzyme (ECE) induced in rats with an atherogenic diet. On the other hand, AR augmented the vascular expression of endothelial nitric oxide synthase (ecNOS) and restored vascular nitric oxide (NO) production. Furthermore, AR suppressed the elevated expression of vascular nuclear factor-kappaB (NF-kappaB) p65 as well as adhesion molecules, including intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in rats fed with an atherogenic diet. Also, AR decreased endothelial expression of ICAM-1 and ET-1 in aorta. These results suggest that AR suppresses the development of atherosclerosis in the atherogenic-diet rat model through inhibiting vascular expressions of proinflammatory and adhesion molecules via the regulation of nitric oxide and endothelin system.