Treatment of NCBAE (H) and NCBAE (M) caused reduction in the development of SBP in 2K1C rats (P < 0.01, P < 0.05, resp., Figure 2).
As shown in the figure, a remarkably thickened left ventricular wall was observed in 2K1C hypertensive group compared with sham-operated group, while this change was alleviated after six-week NCBAE treatments.
Compared with the 2K1C group, NCBAE (H) treatment and Ator treatment decreased LVW/BWratio significantly.
Moreover, cardiomyocyte CSA significantly increased in 2K1C rats compared with the sham-operated group (P < 0.01, Figures 4 and 5).These pathological changes were reduced significantly with NCBAE (H) treatment and Ator treatment (P < 0.01, Figures 4 and 5) compared with 2K1C group.
Treatment with NCBAE (H) and Ator for 6 weeks resulted in a significant increase in serum NO level compared with 2K1C group (P < 0.01, Figure 6).
Importantly, both the activation of caspase-3 and the downregulation of Bcl2 observed in 2K1C hypertensive hearts were significantly attenuated by NCBAE (H), NCBAE (M), and Ator (P < 0.01, Figures 7(a) and 7(b)), suggesting that the modulation of apoptotic process by NCBAE might contribute to the beneficial effect on 2K1C hypertensive hearts.
During six-week NCBAE treatments, we observed that the extract showed an antihypertensive effect, decreased SBP of hypertensive rats compared with 2K1C group.
To gain more insight into the mechanism of the NCBAE function, we examined the cardiac protein expression of Bcl-2 and caspase-3.
This cardiac injury and pathological remodeling can be reversed to some degree by NCBAE treatment.
Caption: Figure 1: Identification of linarin (a) and [beta]-sitosterol (b) in NCBAE by UPLC-MS method.
Caption: Figure 4: Effects of NCBAE on cardiac hypertrophy (representative pictures of myocardium stained with H&E, magnification: 400x).
Caption: Figure 6: Inhibitory effects of treatment with NCBAE on 2K1C-induced reduction in serum NO and elevation of serum LDH in rats.