Impact of ADMA (asymmetric dimethylarginine) on physiology with respect to diabetes mellitus and respiratory system BEAS-2B cells (human bronchial epithelial cells).

摘要: Objectives Asymmetric dimethylarginine (ADMA) is a non-selective nitric oxide (NO) synthase inhibitor associated with cardiovascular and metabolic disorders. This study aimed to investigate ADMA respect both diabetes respiratory disease. Methods Glucose was determined by hexokinase method, insulin radioimmunoassay. Griess test used for NO assay cytokinines were assayed ELISA. Ciliary beat frequency high speed video using microscope. Key findings ADMA induced an increase in blood glucose plasma levels rats; the ratio of these effects indicates induction diabetic situation (insulin resistance). l-arginine increased initially slightly decreased insulin. A pretreatment abolished effects. shows similar vitro (insulin-secreting cell line, INS-1 cells). production NO, which reversed (INS-1 also reduced positively modulated various substances, namely metformin, ciglitazone, losartan nateglinide, but nevertheless inhibited release compounds. stimulated cytokines such as interleukin (IL-6) macrophage inflammatory protein-2 (MIP-2) (rat IL-8 analogue) from cells. 5-Aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR), direct adenosine monophosphate protein kinase (AMPK) activator anti-inflammatory agent, cytokine release. In contrast parameters, had no effect on system (cytokine secretion BEAS-2B cells (IL-8, regulated activation, normal T expressed secreted, tumour necrosis factor-α), ciliary smooth muscle contraction rat trachea). Conclusions ADMA has pathophysiological impact leading system.