[Inhibitory effect of nitric oxide-induced total ginsenosides on right ventricular hypertrophy in rats].

Objective: To observe the effect of total ginsenosides (TG) on right ventricular hypertrophy induced by monocrotaline (MCT) in rats, and study its relationship with the nitric oxide pathway.

Method: Male Sprague Dawley rats were randomly divided into the control group, the MCT model group, TG-treated (20, 40, 60 mg kg-1 d-1) groups, and the L-arginine (L-arg) th NO release, T + L-N and L-a + L-N groups were wi th NOS into study TG's effect 200 mg kg-1 d-1 group. Besides, and its relationship wi also set, intraperitoneally injected with TG 40 mg kg-1 d -1 and L-arg 200 mg kg-1 - d-1, and orally administered hibitor L-NAME 20 mg kg-1 d-1. After all of the groups were given drugs for 18 d, their right ventricular peak systolic pressure (RVSP) ventricular hypertrophy index (RVHI) and RVW/BW were determined. Ultra-structure of myocardial cells was observed with transmission electron microscope. The NO2 -/NO3 - content in myocardial tissues were detected with the nitrate reduction method. ANF and eNOS mRNA expressions in right ventricle tissues were detected by using real-time RT-PCR.

Result: Low, middle and high doses of TG and L-arg preventive administration could significantly reduce RVSP, RVHI, RVW/BW and ANF mRNA expressions (P < 0. 05) , and ameliorate cellular mitochondrial swelling and degeneration. L-NAME could prevent the effect of L-arg on above indexes, whereas L-NAME of the same dose could not impact the reducing effect of TG 40 mg kg -1 on above indexes. TG 60 mg kg -1 could raise eNOS mRNA expression, but TG 20 mg kg-1 and 40 mg kg-1 showed no effect.

Conclusion: TG can significantly attenuate MCT-induced right cardiac hypertrophy in rats. Its anti-hypertrophic effect is partially realized through NO.