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. 2022 Mar 31;9:881372. doi: 10.3389/fcvm.2022.881372

FIGURE 1.

FIGURE 1

CagA+ Helicobacter pylori, not CagA– H. pylori infection, led to significant endothelial dysfunction, and promoted the development of atherosclerosis. ACh-induced aortic relaxation was significantly reduced in male C57BL/6 mice after 1 week (A) or 12 weeks (B) of CagA+ H. pylori infection compared with control, while no change in ACh-induced aortic relaxation in mice with CagA– H. pylori infected was observed (C,D); (E–I) Representative images and quantification of Oil-red O-stained whole aorta of LDLR–/– mice with PBS, CagA+ H. pylori or CagA– H. pylori infection after 3, 5, and 12 weeks of high-fat diet (HFD). (J–N) Representative images of cross-section histological and quantification of atherosclerotic lesions in aortic roots. NC(1/2): normal control; ACh: acetylcholine; CagA+Hp: CagA+ H. pylori; CagA– Hp: CagA– H. pylori. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01 by t-test, N = 8–10 mice for each group at each time point.