动物造模,阿司匹林 z-bo 2020-09-09 401

　　Objective: To explore the regulatory effect of aspirin on related mechanisms in salt-sensitive hypertensive rats?

　　Method: administer the low salt (0.12% NaCl, LS) and high salt (8% NaCl, HS) of salt-sensitive rats (DahlSS) and control salt-tolerant rats (SS-13BN) 2 months ago. , High salinity and aspirin oral gavage ((10mg/(kg·d)), HS + ASA) for up to 8 weeks, continuous measurement of cuff artery blood pressure. After 8 weeks, the common carotid artery was cannulated to measure the arterial blood pressure of the rat. Real-time fluorescence quantitative PCR was used to detect the expression of inflammatory factors IL-6, IL-1β and TNF-α in kidney tissue, and immunofluorescence was used to detect skin M2 macrophages. Express eNOS? vWF, the vascular function protein represented by Western blot?

　　Results: After high salt intake in DahlSS rats, blood pressure increased significantly, and inflammatory factors and vascular vWF factors in the kidney tissue increased significantly? The number of skin M2 macrophages and the expression of eNOS in blood vessels were significantly reduced. Aspirin can effectively reduce the inflammatory response and vascular function damage in Dahl SS rats caused by salt, but does SS-13BN rats not have the above situation?

　　Conclusion: Does aspirin inhibit the high salt-induced inflammatory response in DahlSS rats through its antiplatelet function, damaging blood vessel function and developing hypertension?