Andrographolide (ANDRO) is a diterpene lactone compound with extensive biological effects, such as antibacterial, antitumor and treatment of cardiovascular diseases. Until now, studies on the pharmacological functions of ANDRO are still in progress. However, little is known about the gene expression profile and calcium response of endothelial cells to ANDRO. In this study, we used a microarray technology to investigate the gene expression responses in primary rat myocardium microvascular endothelial cells treated with 10 μg/mL ANDRO. The expression of caveolin-1 and 1-phosphatidylinositol 4, 5-bisphosphate phosphodiesterase δ3 was verified by RT-PCR and western blot. In addition, we investigated the effect of ANDRO on intracellular calcium induced by exogenous adenosine triphosphate and on inflammatory response induced by lipopolysaccharide. Results showed that ANDRO treatment induced an abundance of differential expressed genes, exhibiting a multitarget regulatory effect. ANDRO significantly decreased caveolin-1 and phosphodiesterase δ3 expression, lipopolysaccharide-induced IL-6 and TNF-α levels and expression of several chemokine genes, which are associated with reducing inflammation response and decreasing calcium release without affecting normal endothelia cell function, suggesting that ANDRO may be a potential candidate to treat cardiovascular diseases with less toxicity.

Endothelial cells are believed to play an important role in response to virus infection. Our previous microarray analysis showed that H9N2 virus infection and inactivated viral particle inoculation increased the expression of interferon-inducible transmembrane protein 1 (IFITM1) in human umbilical vein endothelial cells (HUVECs). In present study, we deeply investigated the expression patterns of IFITM1 and IFITM1-mediated antiviral response induced by H9N2 virus infection and inactivated viral particle inoculation in HUVECs. Epithelial cells that are considered target cells of the influenza virus were selected as a reference control. First, we quantified the expression levels of IFITM1 in HUVECs induced by H9N2 virus infection or viral particle inoculation using quantitative real-time PCR and western blot. Second, we observed whether hemagglutinin or neuraminidase affected IFITM1 expression in HUVECs. Finally, we investigated the effect of induced-IFITM1 on the antiviral state in HUVECs by siRNA and activation plasmid transfection. Both H9N2 virus infection and viral particle inoculation increased the expression of IFITM1 without elevating the levels of interferon-ɑ/β in HUVECs. HA or NA protein binding alone is not sufficient to increase the levels of IFITM1 and interferon-ɑ/β in HUVECs. IFITM1 induced by viral particle inoculation significantly decreased the virus titers in culture supernatants of HUVECs. Our results showed that inactivated viral particle inoculation increased the expression of IFITM1 at mRNA and protein levels. Moreover, the induction of IFITM1 expression mediated the antiviral state in HUVECs.