fig4

Figure 4. Caproic acid ameliorates angiotensin II-induced arteriosclerosis and vascular dysfunction in mice. (A) Schematic of the in vivo experimental design. Young mice were treated with either PBS (i.h.) or Na-C6 (i.h.) and infused with AngII via osmotic pump for 4 weeks, followed by sacrifice and tissue analysis. (B) Aortic arch PWV, (C) SBP, and (D) pulse pressure in AngII-infused mice with or without Na-C6 treatment (n = 5 per group). (E) Representative H&E, Masson’s trichrome, and EVG staining of thoracic aorta sections from AngII and AngII + Na-C6 mice. Scale bar, 100 μm. (F) Quantification of aortic medial thickness, (G) aortic fibrosis level (fold change), and (H) elastin breaks per section in the AngII and AngII + Na-C6 mice (n = 5 per group). (I) Representative Western blot images showing the expression of senescence markers p53, p21^Waf1/cip1, and p16^INK4A in aorta tissues. GAPDH was used as the loading control. (J-L) Densitometric quantification of (J) p53, (K) p21^Waf1/cip1, and (L) p16^INK4A protein levels in aorta, normalized to GAPDH (n = 4 per group). Na-C6: Sodium caproate; PWV: pulse wave velocity; SBP: systolic blood pressure. Data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. AngII group (unpaired two-tailed Student’s t-test). (A) was created in BioRender. Xie, Y. (2026) https://BioRender.com/bmztl73.