AB184. Icariside II induces NO production in human cavernous endothelial cells via the activation of eNOS by miR-155

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Objective To investigate the status miR-155 and its targeting eNOS under the stimulation of glucose and age-BSA and to explore the effect of icariside II (ICA II) on the diabetic endothelial dysfunction of human cavernous endothelial cells (HCECs) by using the miR-155 pathway. Methods Purified HCECs were divided into three groups: normal group + BSA (NC group), Glucose + Age-BSA group (DM group), ICA II treatment group (DM + ICA II group). Western blot to detect the expression of eNOS and RAGE protein expression; immunofluorescence assay to detect the NO production; real time PCR to detect the expression of miR-155 and eNOS. Overexpression of miR-155 was performed in HCECs with or without ICA II interference. Results Under the diabetic induction, the expression of eNOS in DM group is significantly reduced compared with that in NC group and the expression of RAGE in DM group is significantly up-regulated compared with that in NC group (P Conclusions Under the glucose and Age-BSA stimulation, ICA II may induce NO production in HCECs via the activation of eNOS by miR-155 so as to restore the HCECs functions.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.