动物造模,动脉粥样硬化 z-bio 2022-09-23 271

　　Objective: To study the inhibitory effect of adenovirus-mediated adiponectin (APN) overexpression on atherosclerosis (AS) in ApoE-/- mice and its effect on NF-κB signaling pathway.

　　Methods: A total of 120 12-week-old male ApoE-/- mice were divided into adenovirus-free control group and adiponectin intervention group, 60 mice in each group. Tissues were collected by sacrifice of mice at 3 different time points (0 days, 4 weeks, 8 weeks). Automatic biochemical instrument was used to detect blood lipid indexes; ELISA method was used to determine serum APN concentration; Oil red O staining method was used to detect the pathological changes of mouse aortic vascular tissue; Masson staining method was used to detect collagen content and fibrous cap thickness changes in the progressive plaque area; The expressions of APN and NF-κB p65 protein in mouse aortic vessels were detected by immunofluorescence method; the expressions of APN, NF-κB p65 nuclear protein and inflammatory factors were detected by immunoblotting method.

　　RESULTS: APN overexpression inhibited the formation of atherosclerotic plaques in ApoE-/- mice. Compared with the control group, the area of atherosclerotic pathological damage in the adiponectin intervention group was decreased (P<0.01), and the degree of atherosclerotic damage was decreased (P<0.001). At 4 weeks, it was (27.78±8.64) vs (33.02±5.18)%; at 8 weeks, it was (31.58±5.87) vs (52.16±5.79)%. Adiponectin slowed down the increase in serum TC (P<0.001), TG (P<0.001), and LDL-C (P<0.001) concentrations of mice induced by high-fat diet, and normalized blood lipid levels. With the increase of serum adiponectin concentration, it can inhibit the activation of NF-κB pathway and inhibit the expression of NF-κB p65 nuclear protein and inflammatory factors.

　　Conclusion: Adiponectin attenuates the inflammatory response of AS by inhibiting the activation of NF-κB pathway.