Targeted Delivery of Salusin‐α Into Rabbit Carotid Arterial Endothelium Using SonoVue

Abstract

Objectives A new method based on the adhesion of SonoVue to plasmids was assessed to achieve targeted gene delivery into the vascular endothelium. Methods pEGFP‐Salusin‐α and pcDNA3.1‐Salusin‐α plasmids were transfected into the arterial endothelium of different rabbit groups. Western blotting was performed to analyze the expression of EGFP and salusin‐α in the common carotid arteries of rabbits from different groups, and ELISA was performed to detect plasma salusin‐α levels in rabbits from each group; simultaneously, blood parameters of different groups of rabbits were measured. Results Green fluorescence was observed in the right common carotid artery of rabbits transfected with pEGFP‐Salusin‐α, but not in the endothelial cells of not‐transfected control rabbits. The expression of salusin‐α in the transfected animals was higher than that in the control not‐transfected animals (P < .05). In rabbits transfected with pcDNA3.1‐Salusin‐α plasmid, salusin‐α expression was higher than in the not‐transfected control animals (P < .05). However, there was no significant difference in plasma salusin‐α levels between transfected animals and controls (P > .05). Blood parameters were also measured in both groups. Conclusions Our data confirm the establishment of a new method using SonoVue for targeted gene delivery into the arterial endothelium. Our study outcomes propose a new method of intervention in atherosclerosis and a new tool for targeted gene delivery.

Salusin‑α alleviates lipid metabolism disorders via regulation of the downstream lipogenesis genes through the LKB1/AMPK pathway

“…Animal experiments have shown that Salusin-α can also inhibit liver steatosis and reduce plasma TG levels in mice ( 16 ). The authors' research group previously established a new method of targeting the delivery of EGFP-Salusin-α plasmid to the arterial endothelia and demonstrated that Salusin-α can reduce atherosclerosis in rabbits ( 17 ), and it was also demonstrated that Salusin-α may inhibit hepatocyte lipid synthesis through the PPARα/ApoA5/sterol regulatory element binding protein-1c (SREBP-1c) pathway ( 18 ). Nevertheless, the exact mechanism by which Salusin-α affects hepatocyte lipid metabolism remains incompletely understood.…”