自发荧光成像在消化道疾病诊断中的应用

一、自发荧光成像(auto fluorescence imaging,AFI)原理在生物体内某些物质不需外源荧光染料即可受激发发出荧光的现象称自发荧光.在人体组织细胞内富含多种荧光基团,这些荧光基团如胶原蛋白、弹力蛋白、还原型烟酰胺腺嘌呤二核苷酸(NADH)、黄素腺嘌呤二核苷酸(FAD)等主要聚集胃肠道黏膜下层.正常组织和病变组织所透过的自发光强弱不等,影响自发荧光强弱的主要原因与组织内生化成分及其比例有关.

Angiotensin-converting enzyme 2 (ACE2)-angiotensin (1-7) [Ang (1-7)]-Mas constitutes the vasoprotective axis and is demon-strated to antagonize the vascular pathophysiological effects of the classical renin -angiotensin system .We hypothesize that upregulation of ACE2-Ang (1-7) signaling protects endothelial function through reducing oxidative stress , thus resulting in beneficial outcome in di-abetes.Ex vivo treatment with Ang (1-7) augmented endothelium-dependent relaxation (EDR) in renal arteries from diabetic patients . Both Ang (1-7) infusion via osmotic pump (500 ng? kg -1? min-1 ) for 2 weeks and exogenous ACE 2 overexpression mediated by ad-enoviral ACE2 via tail vein injection rescued the impaired EDR and flow-mediated dilatation ( FMD) in db/db mice.Diminazene acetu-rate treatment (15 mg? kg-1? d-1 ) activated ACE2, increased the circulating Ang (1-7) level, and augmented EDR and FMD in db/db mouse arteries.In addition, activation of the ACE2-Ang (1-7) axis reduced reactive oxygen species (ROS) overproduction de-termined by dihydroethidium staining , CM-H2DCFDA fluorescence imaging , and chemiluminescence assay in db/db mouse aortas and also in high-glucose-treated endothelial cells .Pharmacological benefits of ACE 2-Ang ( 1-7 ) upregulation on endothelial function were confirmed in ACE2 knockout mice both ex vivo and in vitro.We elucidate that the ACE2-Ang (1-7)-Mas axis serves as an important signal pathway in endothelial cell protection in diabetic mice , especially in diabetic human arteries .In summary, endogenous ACE2-Ang (1-7) activation or ACE2 overexpression preserves endothelial function in diabetic mice through increasing nitric oxide bioavail -ability and inhibiting oxidative stress , suggesting the therapeutic potential of ACE 2-Ang(1-7) axis activation against diabetic vasculop-athy.