Objective: To study the inhibitory effect of adenovirus-mediated adiponectin (APN) overexpression on ApoE-/- mouse atherosclerosis (AS) and its influence on NF-κB signaling pathway.
Method: 120 12-week-old male ApoE-/- mice were divided into an empty adenovirus control group and an adiponectin intervention group, with 60 in each group. Mice were sacrificed at 3 different time points (0 days, 4 weeks, 8 weeks) and tissues were collected. Automated biochemical analyzer to detect blood lipid indicators; enzyme-linked immunosorbent assay method to determine serum APN concentration; oil red O staining method to detect pathological changes of mouse aortic vascular tissue; collagen content in progressive plaque area and fiber Masson staining method Changes in the thickness of sexual cap; immunofluorescence method was used to detect the expression of APN and NF-κBp65 protein in mouse aortic vessels; Western blot was used to detect APN in aortic vessels. We tested the expression of NF-κBp65 nuclear protein and inflammatory factors.
"Result: APN overexpression inhibited the formation of atherosclerotic plaques in ApoE-/- mice. Compared with the control group, the adiponectin intervention group reduced the atherosclerotic lesion area (P \u003cu\→ u0.01c0.01) and (p \u003cu\→ u0.001c0.001). Use Global Oil Red O staining to determine the percentage of surface damage to the container. At 4 weeks, it was (27.78±8.64)% (33.02±5.18)%; at 8 weeks, it was (31.58±5.87)% (52.16±5.79)%. Adiponectin slowed down the increase in serum TC (P\u003c0.001), TG (P\u003c0.001) and LDL-C (P\u003c0.001) concentrations in mice caused by high-fat diet, and normalized blood lipid levels. Elevated serum adiponectin levels can block the activation of the NF-κB pathway and inhibit the expression of NF-κB p65 nuclear protein and inflammatory factors.
Conclusion: Adiponectin reduces the inflammatory response of AS by inhibiting the activation of NF-κB pathway.