Effects of Xin‐Ji‐Er‐Kang on Anticardiovascular Remodeling in L‐NAME Induced Hypertensive Mice and Its Potential Mechanisms

Figures

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  Figure 1. Effects of XJEK on SBP in L-NAME induced hypertensive mice during a 8 wk period. Nine time points of SBP were determined using tail-cuff apparatus measurement in each group. (mean ± SD, n = 8~10). ∗∗P < 0.01 vs. Control group; ##P < 0.01 vs. L-NAME group.

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  Figure 2. Effects of XJEK on HW/BW, cardiomyocyte CSA, and cardiomyocyte long axis in L-NAME induced hypertensive mice. (a) Representative images of histological section of cardiomyocyte long axis (HE staining, 400x); (b) representative images of histological section of cardiomyocyte long axis (HE staining, 400x); (c) ratio of heart to body weight (HW/BW, mg/g); (d) summary of CSA results analyzed by Image J. (mean ± SD, n = 8~10). (1) Control group; (2) L-NAME group; (3) L-NAME + XJEK 7.5 g/kg group; (4) L-NAME + Irbesartan 40 mg/kg group. ∗∗P < 0.01 versus control group; ##P < 0.01 versus L-NAME group.

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  Figure 3. Effects of XJEK on cardiac fibrosis in L-NAME induced hypertensive mice. (a) Representative images of histological sections of myocardial fibrosis with VG staining (400x); (b) representative images of histological sections of perivascular fibrosis with VG staining (400x); (c) quantification results of myocardial fibrosis; (d) quantification results of perivascular fibrosis analyzed by Image J as % (mean ± SD, n = 8~10). (1) Control group; (2) L-NAME group; (3) L-NAME + XJEK 7.5 g/kg group; (4) L-NAME + Irbesartan 40 mg/kg group. ∗∗P < 0.01 versus control group; ##P < 0.01 versus L-NAME group.

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  Figure 4. Representative figure of thoracic remodeling in different groups (HE staining, 100x). (1) Control group; (2) L-NAME group; (3) L-NAME + XJEK 7.5 g/kg group; (4) L-NAME + Irbesartan 40 mg/kg group.

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  Figure 5. Effects of XJEK on aorta vasodilation in L-NAME induced hypertensive mice (mean ± SD, n = 8~10). ∗∗P < 0.01 versus control group; #P < 0.05 and ##P < 0.01 versus L-NAME group.

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  Figure 6. Treatment with XJEK alleviated endothelial dysfunction (mean ± SD, n = 8~10). (a) eNOS (U/L); (b) NO (μmol/L); (c) ADMA (nmol/L). ∗∗P < 0.01 versus control group; #P < 0.05 versus L-NAME group. ##P < 0.01 versus L-NAME group.

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  Figure 7. Effects of XJEK on SOD (a) and MDA (b) contents in L-NAME induced hypertensive mice.∗∗P < 0.01 versus control group; #P < 0.05 and ##P < 0.01 versus L-NAME group.

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  Figure 8. Endothelial nitric oxide synthase protein expression determined with immunohistological staining in interstitial tissues of myocardium and intramuscular arteries in hearts (200x, 400x) (mean ± SD, n = 8~10). Compared with control group, the eNOS protein expression levels in hearts of L-NAME group decreased significantly, which could be prevented by treatment with XJEK, just as the positive drug Irbesartan did.

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  Figure 9. Effects of XJEK on eNOS expression (mean ± SD, n = 3). ∗P < 0.05 versus control group; #P < 0.05 versus L-NAME group.