动物造模,盐敏感性高血压 z-bio 2021-02-03 346

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

　　Method: Give two-month-old salt-sensitive rats (DahlSS) and control salt-tolerant rats (SS-13BN) respectively. Low salt (0.12% NaCl, LS), high salt (8% NaCl, HS), high salt and aspirin tube ((10 mg/(kg? D)), HS + ASA), up to 8 weeks, continuous tail sleeve After 8 weeks of formal arterial blood pressure measurement, the rat’s arterial blood pressure was measured by intubation into the common carotid artery, and the expression of inflammatory factors IL-6 and IL was detected by real-time PCR. Detect -1β, kidney tissue TNF-α and skin M2 macrophages by immunofluorescence. ENOS, is this a typical vascular function protein obtained by Western blot analysis? Express vWF?

　　Result: After feeding DahlSS rats with high salt, does the blood pressure increase significantly, and the expression of renal tissue inflammatory factors and vascular vWF factors increase significantly? The number of skin M2 macrophages and the expression of eNOS in blood vessels were significantly reduced. Aspirin can effectively improve blood pressure caused by blood pressure. DahlSS rats have abnormally high salt, inflammation and vascular function, but have SS-13BN rats encountered the above situation?

　　 Conclusion: Aspirin inhibits the inflammatory response induced by high salt in DahlSS rats through antiplatelet function, and inhibits vascular damage and hypertension?